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1. Secondino S, Citterio A, Pedrazzoli P, Funaioli C, Scialfa GG, Siena S: Neuroimaging abnormalities in adult medulloblastoma undergoing intensified therapy. Anticancer Res; 2008 Nov-Dec;28(6B):3991-2
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  • [Title] Neuroimaging abnormalities in adult medulloblastoma undergoing intensified therapy.
  • We report on radiological abnormalities resembling recurrent tumor in adult medulloblastoma receiving intensified chemotherapy and radiotherapy.
  • Evidence provided in this paper confirms previous reports in the pediatric population and suggests that neuroradiologist and medical oncologists should be aware of new possible radiological findings related to aggressive treatments for brain tumors.
  • [MeSH-major] Brain Neoplasms / diagnosis. Medulloblastoma / diagnosis
  • [MeSH-minor] Adult. Female. Humans. Magnetic Resonance Imaging

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  • (PMID = 19192661.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
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2. Figols-Ladrón de Guevara J, Lafuente-Sánchez JV: [The medulloblastoma]. Rev Neurol; 2006 Aug 16-31;43(4):213-7
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  • [Title] [The medulloblastoma].
  • INTRODUCTION AND DEVELOPMENT: Medulloblastoma is a cerebellar small cell tumor, whose ancestor cell has not been yet identified in the human normal embriology: its exact origin is, in fact, still unknown.
  • Nevertheless, one of the most acceptable possibilities facing the origin of the tumor is the remaining rests of cerebellar outer granular sheet.
  • It is a predominantly infantile tumor, less frequent in young adults, and World Health Organization (WHO) classification has assignated grade IV of malignancy.
  • In this publication of the WHO, medulloblastomas have been subclassified into: classic, desmoplastic, medulloblastomas with extensive nodularity and advanced neuronal differentiation and large cell medulloblastomas.
  • [MeSH-major] Brain Neoplasms. Medulloblastoma
  • [MeSH-minor] Adult. Cerebellum / pathology. Chromosomes, Human, Pair 17. Diagnosis, Differential. Humans. Isochromosomes. Prognosis. Survival Rate

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  • (PMID = 16883510.001).
  • [ISSN] 0210-0010
  • [Journal-full-title] Revista de neurologia
  • [ISO-abbreviation] Rev Neurol
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Spain
  • [Number-of-references] 17
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3. Ferretti E, De Smaele E, Po A, Di Marcotullio L, Tosi E, Espinola MS, Di Rocco C, Riccardi R, Giangaspero F, Farcomeni A, Nofroni I, Laneve P, Gioia U, Caffarelli E, Bozzoni I, Screpanti I, Gulino A: MicroRNA profiling in human medulloblastoma. Int J Cancer; 2009 Feb 1;124(3):568-77
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  • [Title] MicroRNA profiling in human medulloblastoma.
  • Medulloblastoma is an aggressive brain malignancy with high incidence in childhood.
  • However, no data are yet available on human primary medulloblastomas.
  • A high throughput microRNA expression profiles was performed in human primary medulloblastoma specimens to investigate microRNA involvement in medulloblastoma carcinogenesis.
  • We identified specific microRNA expression patterns which distinguish medulloblastoma differing in histotypes (anaplastic, classic and desmoplastic), in molecular features (ErbB2 or c-Myc overexpressing tumors) and in disease-risk stratification.
  • MicroRNAs expression profile clearly differentiates medulloblastoma from either adult or fetal normal cerebellar tissues.
  • Only a few microRNAs displayed upregulated expression, while most of them were downregulated in tumor samples, suggesting a tumor growth-inhibitory function.
  • This property has been addressed for miR-9 and miR-125a, whose rescued expression promoted medulloblastoma cell growth arrest and apoptosis while targeting the proproliferative truncated TrkC isoform.
  • In conclusion, misregulated microRNA expression profiles characterize human medulloblastomas, and may provide potential targets for novel therapeutic strategies.
  • [MeSH-major] Biomarkers, Tumor / genetics. Cerebellar Neoplasms / genetics. Gene Expression Profiling. Medulloblastoma / genetics. MicroRNAs

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  • [Copyright] Copyright (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18973228.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] Italy / Telethon / / GGP07118
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MicroRNAs; EC 2.7.10.1 / Receptor, trkC
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4. Holland H, Koschny R, Krupp W, Meixensberger J, Bauer M, Schober R, Kirsten H, Ganten TM, Ahnert P: Cytogenetic and molecular biological characterization of an adult medulloblastoma. Cancer Genet Cytogenet; 2007 Oct 15;178(2):104-13
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  • [Title] Cytogenetic and molecular biological characterization of an adult medulloblastoma.
  • Medulloblastoma is a malignant invasive embryonal tumor, occurring in children mainly.
  • It is rare in adults (<1% of adult brain tumors), and so comprehensive cytogenetic and molecular biological data on adult medulloblastomas are very limited.
  • We performed comprehensive cytogenetic analyses of an adult medulloblastoma, WHO grade IV, using trypsin-Giemsa staining (GTG-banding), multicolor fluorescence in situ hybridization (M-FISH), and locus-specific FISH, complemented by molecular karyotyping using high-density single nucleotide polymorphism (SNP) arrays.
  • Molecular karyotyping by SNP array confirmed chromosomal changes -2p, -10q, -16q, and -Xq and revealed de novo partial uniparental disomy 1q and 9q.
  • Applying an upcoming therapeutic approach, we found that primary medulloblastoma cells were resistant to TRAIL, a novel anticancer cytokine, but could be efficiently sensitized by cotreatment with the proteasome inhibitor bortezomib.
  • Bortezomib-TRAIL cotreatment may serve as a powerful therapeutic option for medulloblastoma patients.
  • [MeSH-major] Cerebellar Neoplasms / genetics. Medulloblastoma / genetics
  • [MeSH-minor] Adult. Child. Chromosome Aberrations. Chromosome Banding. Female. Flow Cytometry. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Matrix Metalloproteinase 2 / genetics. Phosphopyruvate Hydratase / genetics. Polymorphism, Single Nucleotide. Synaptophysin / genetics

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  • (PMID = 17954265.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Synaptophysin; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 4.2.1.11 / Phosphopyruvate Hydratase
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5. Viana-Pereira M, Almeida I, Sousa S, Mahler-Araújo B, Seruca R, Pimentel J, Reis RM: Analysis of microsatellite instability in medulloblastoma. Neuro Oncol; 2009 Oct;11(5):458-67
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  • [Title] Analysis of microsatellite instability in medulloblastoma.
  • Medulloblastoma is the most common malignant brain tumor in children.
  • The presence of microsatellite instability (MSI) in brain tumors, particularly medulloblastomas, has not been properly addressed.
  • The aim of the present study was to evaluate the role of MSI in medulloblastoma carcinogenesis.
  • This study is the most comprehensive analysis of MSI in medulloblastomas to date.
  • We observed the presence of MSI together with mutations of MSI target genes in a small fraction of cases, suggesting a new genetic pathway for a role in medulloblastoma development.
  • [MeSH-major] Biomarkers, Tumor / genetics. Cerebellar Neoplasms / genetics. Medulloblastoma / genetics. Microsatellite Instability
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. DNA Methylation. DNA Mutational Analysis. Female. Humans. Immunohistochemistry. Infant. Male. Middle Aged. Polymerase Chain Reaction. Polymorphism, Single-Stranded Conformational. Young Adult

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  • (PMID = 19179424.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Other-IDs] NLM/ PMC2765336
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6. Padovani L, André N, Carrie C, Muracciole X: [Childhood and adult medulloblastoma: what difference?]. Cancer Radiother; 2009 Oct;13(6-7):530-5
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  • [Title] [Childhood and adult medulloblastoma: what difference?].
  • [Transliterated title] Le médulloblastome de l'enfant et de l'adulte: quelle différence?
  • Medulloblastoma is the most frequent childhood brain tumor (30%) but account only for less than 1% of adult brain tumor.
  • Due to the rarety in adult population, no prospective studies and few data about late effects are available.
  • Adult medulloblastoma is a therapeutic challenge and their therapeutic strategies are similar to pediatric protocols.
  • In order to improve the understanding of adult disease and to homogenize the treatment, National Cancer Institute (INCa) stimulated the creation of web conference to discuss each case prospectively and to propose a protocol of treatment.
  • A better comprehension of biological processes and abnormal cellular signalling pathways involved in medulloblastoma pathogenesis had led toward a new prognostic classification to adapt the therapeutic strategy and gives hope of new therapeutic tools.
  • [MeSH-major] Cerebellar Neoplasms / pathology. Medulloblastoma / pathology
  • [MeSH-minor] Adult. Age Factors. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Brain Neoplasms / epidemiology. Child. Cognition Disorders / epidemiology. Cognition Disorders / etiology. Combined Modality Therapy. France / epidemiology. Humans. Incidence. Molecular Biology / methods. Radiotherapy / adverse effects. Radiotherapy / methods. Surgical Procedures, Operative

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  • (PMID = 19713143.001).
  • [ISSN] 1769-6658
  • [Journal-full-title] Cancer radiothérapie : journal de la Société française de radiothérapie oncologique
  • [ISO-abbreviation] Cancer Radiother
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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7. Sousa R, Sá G, Reimão S, Lopes L, Ruivo J, Albuquerque L, Campos J: [Adult cerebellar medulloblastoma: imaging findings in eight cases]. Acta Med Port; 2006 Nov-Dec;19(6):466-70
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  • [Title] [Adult cerebellar medulloblastoma: imaging findings in eight cases].
  • Medulloblastoma is a brain tumor of neuroepithelial origin, frequent in children but rare in adults.
  • The imaging pattern is well studied in the pediatric group thought there is controversy about the imaging characteristics in adults.
  • We report CT and MRI imaging findings of 8 adult patients with cerebellar medulloblastoma.
  • The imaging findings of medulloblastomas in adults are unspecific and different from those in child.
  • They should be considered in the differential diagnosis of cerebellar tumor in adults, especially if they are hyperdense on CT, with well defined margins, with superficial extension and with dural involvement.
  • [MeSH-major] Cerebellar Neoplasms / pathology. Cerebellar Neoplasms / radiography. Medulloblastoma / pathology. Medulloblastoma / radiography
  • [MeSH-minor] Adolescent. Adult. Cerebellum / pathology. Cerebellum / radiography. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Tomography, X-Ray Computed

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  • (PMID = 17583605.001).
  • [ISSN] 1646-0758
  • [Journal-full-title] Acta médica portuguesa
  • [ISO-abbreviation] Acta Med Port
  • [Language] por
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Portugal
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8. Howes TL, Buatti JM, Kirby PA, Carlisle TL, Ryken TC: Radiation induced adult medulloblastoma: a case report. J Neurooncol; 2006 Nov;80(2):191-4
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  • [Title] Radiation induced adult medulloblastoma: a case report.
  • Adult medulloblastoma is a rare intracranial tumor.
  • Our patient is a 61 year old woman treated with cranial irradiation 15 years previously for a low grade astrocytoma in the left posterior temporal lobe that was recently diagnosed with medulloblastoma in the right cerebellum.
  • This is the first reported case of radiation induced adult medulloblastoma.
  • [MeSH-major] Cerebellar Neoplasms / etiology. Medulloblastoma / etiology. Neoplasms, Radiation-Induced / pathology
  • [MeSH-minor] Astrocytoma / radiotherapy. Brain Neoplasms / radiotherapy. Craniotomy. Female. Humans. Magnetic Resonance Imaging. Middle Aged. Neurosurgical Procedures. Temporal Lobe / pathology

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  • (PMID = 16710747.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
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9. Herrlinger U, Steinbrecher A, Rieger J, Hau P, Kortmann RD, Meyermann R, Schabet M, Bamberg M, Dichgans J, Bogdahn U, Weller M: Adult medulloblastoma: prognostic factors and response to therapy at diagnosis and at relapse. J Neurol; 2005 Mar;252(3):291-9
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  • [Title] Adult medulloblastoma: prognostic factors and response to therapy at diagnosis and at relapse.
  • Adult medulloblastoma is a rare tumor with few retrospective studies published so far.
  • This study reports therapy and outcome in all adult (>or=16 years old) medulloblastoma (n=34) and supratentorial primitive neuroectodermal tumor (PNET) patients (n=2) treated in 2 neuro-oncological centers between 1976 and 2002.
  • In conclusion, adjuvant chemotherapy may prolong survival in adult medulloblastoma patients.
  • As in pediatric medulloblastoma patients, primary infiltration of the floor of the 4(th) ventricle indicates a poor prognosis.
  • [MeSH-major] Cerebellar Neoplasms / therapy. Medulloblastoma / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Analysis of Variance. Combined Modality Therapy. Demography. Disease Progression. Disease-Free Survival. Dose-Response Relationship, Radiation. Drug Therapy / methods. Female. Humans. Male. Middle Aged. Radiotherapy, High-Energy / methods. Recurrence. Regression Analysis. Retrospective Studies. Risk Factors. Time Factors. Treatment Outcome

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  • (PMID = 16189725.001).
  • [ISSN] 0340-5354
  • [Journal-full-title] Journal of neurology
  • [ISO-abbreviation] J. Neurol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] Germany
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10. Menon G, Krishnakumar K, Nair S: Adult medulloblastoma: clinical profile and treatment results of 18 patients. J Clin Neurosci; 2008 Feb;15(2):122-6
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  • [Title] Adult medulloblastoma: clinical profile and treatment results of 18 patients.
  • The objective of this article is to examine the clinicoradiological features and surgical outcomes of adult patients (>16 years) with medulloblastoma.
  • An attempt was made to identify the predictors of poor outcome and assess patterns of relapse and to compare these with pediatric medulloblastoma.
  • Retrospective case record analyses were performed on 18 adults (>16 years) and 79 children (<16 years) operated upon after January 1990, who had at least 5 years of follow-up.
  • The tumor was located in the vermis in 12 patients (66.6%) and in the cerebellar hemisphere in six (16.6%).
  • In spite of recent advances in management, patients with medulloblastoma still have a poor prognosis.
  • However, adults fared better than children.
  • Vermian location had a better outcome in adults, but not in children.
  • Desmoplastic variant histology was not observed to be a significant prognostic factor in the adult group while brain stem invasion carried a poor prognosis.
  • [MeSH-major] Cerebellar Neoplasms / therapy. Clinical Trials as Topic. Medulloblastoma / therapy
  • [MeSH-minor] Adolescent. Adult. Age Factors. Female. Humans. Male. Middle Aged. Prognosis. Retrospective Studies. Statistics, Nonparametric. Treatment Outcome

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  • (PMID = 18078755.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Scotland
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11. Yoshimura J, Nishiyama K, Fukuda M, Watanabe M, Igarashi H, Fujii Y: Adult cerebellopontine angle medulloblastoma originating in the pons mimicking focal brainstem tumor. J Neuroimaging; 2009 Oct;19(4):385-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult cerebellopontine angle medulloblastoma originating in the pons mimicking focal brainstem tumor.
  • We herein report a rare case of cerebellopontine angle (CPA) medulloblastoma originating in the brainstem that demonstrated a very unusual clinical presentation and radiological appearances.
  • A small non-enhanced lesion having minimal mass effect in the right CPA was identified by using a 1.5-tesla-MR system, whose size remained almost unchanged a year.
  • MR spectroscopic images using a 3-tesla system revealed a high ratio of choline-to-N-acetylaspartate in the region of interest in comparison to the contra-lateral side.
  • The histopathological diagnosis was medulloblastoma.
  • MR spectroscopic imaging is considered to be quite useful for the management of this rare type of brainstem tumor.
  • [MeSH-major] Brain Stem Neoplasms / pathology. Cerebellopontine Angle / pathology. Infratentorial Neoplasms / pathology. Medulloblastoma / pathology. Pons / pathology
  • [MeSH-minor] Adult. Aspartic Acid / analogs & derivatives. Aspartic Acid / metabolism. Choline / metabolism. Diagnosis, Differential. Female. Follow-Up Studies. Functional Laterality. Humans. Magnetic Resonance Imaging. Magnetic Resonance Spectroscopy

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  • (PMID = 19021841.001).
  • [ISSN] 1552-6569
  • [Journal-full-title] Journal of neuroimaging : official journal of the American Society of Neuroimaging
  • [ISO-abbreviation] J Neuroimaging
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 30KYC7MIAI / Aspartic Acid; 997-55-7 / N-acetylaspartate; N91BDP6H0X / Choline
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12. Giordana MT, D'Agostino C, Pollo B, Silvani A, Ferracini R, Paiolo A, Ghiglione P, Chiò A: Anaplasia is rare and does not influence prognosis in adult medulloblastoma. J Neuropathol Exp Neurol; 2005 Oct;64(10):869-74
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  • [Title] Anaplasia is rare and does not influence prognosis in adult medulloblastoma.
  • Histopathologic grading based on increasing anaplasia predicts clinical behavior of pediatric medulloblastomas.
  • The present study was aimed at grading 86 medulloblastomas of adult patients (aged 18 and older) by anaplasia and analyzing the predictive power.
  • Severe nuclear pleomorphism was found in 4 of 86 cases; the only large-cell medulloblastoma was from an 18-year-old patient.
  • The histologic spectrum of medulloblastoma in adults is different from that in children.
  • [MeSH-major] Cerebellar Neoplasms / pathology. Medulloblastoma / pathology
  • [MeSH-minor] Adult. Aged. Anaplasia. Female. Humans. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Analysis

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  • (PMID = 16215458.001).
  • [ISSN] 0022-3069
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
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13. Pfister SM, Remke M, Benner A, Werft W, Mendrzyk F, Scheurlen W, Kulozik A, Lichter P, Korshunov A: Use of CDK6 oncogene amplification and 17q gain to predict poor clinical risk groups in adult medulloblastoma. J Clin Oncol; 2009 May 20;27(15_suppl):2030

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  • [Title] Use of CDK6 oncogene amplification and 17q gain to predict poor clinical risk groups in adult medulloblastoma.
  • : 2030 Background: While in children medulloblastoma comprises the most common malignant brain tumor, it accounts for only 1% of intracranial malignancies in adults.
  • The infrequent appearance of MB in adults poses the question, whether these tumors are the same in adults and children in terms of biological and clinical peculiarities.
  • METHODS: Array-CGH was performed for a total 34 adult medulloblastoma samples (>18 years) and results were compared with data from 101 pediatric patients.
  • Selected genomic regions were further investigated by FISH analysis in an independent cohort of 415 samples (112 adult and 303 pediatric).
  • All 146 adult patients received a standard treatment regimen consisting of tumor resection, irradiation of the neuroaxis with 36 Gy, a boost of 20-23 Gy to the posterior fossa, and eight cycles of vincristin, lomustine, and cisplatin.
  • RESULTS: Copy-number gains of chromosome 17q as well as high-level amplifications of CDK6 were identified as significant adverse prognostic markers in adult medulloblastoma.
  • Apart from one exception, CDK6 amplifications were only observed in adult patients (9% in adults versus 0.2 % in children), whereas amplifications of MYC or MYCN were significantly overrepresented in the pediatric cohort, but when present were also associated with dismal prognosis in adults.
  • Based on these results, we propose a molecular staging system for adult medulloblastoma: i) cases with oncogene amplification (10% of cases, 5-year OS = 0%);.
  • CONCLUSIONS: We report on the largest cohort of adult medulloblastoma investigated for genomic imbalances to date.
  • We propose a model for the molecular risk stratification of adult medulloblastoma comprising three distinct genomic risk groups with significantly different survival and tumor biology.

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  • (PMID = 27964634.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Xu P, Pu PY, Kang CS, Jia ZF, Zhou X, Wang GX: [Differential expression of Notch1 and Notch2 in astrocytoma and medulloblastoma]. Zhonghua Bing Li Xue Za Zhi; 2008 Jul;37(7):450-3
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  • [Title] [Differential expression of Notch1 and Notch2 in astrocytoma and medulloblastoma].
  • OBJECTIVE: To detect the differential expression of Notch1 and Notch2 in human astrocytoma and medulloblastoma; and to study the role of Notch1 and Notch2 in the development of both tumors.
  • METHODS: Immunohistochemical staining (SP method) and Western blot analysis were used to detect Notch1 and Notch2 expression in tissue arrays and freshly resected samples of normal brain tissue, astrocytoma and medulloblastoma.
  • RESULTS: Notch1 and Notch2 were negative in normal human brain tissue.
  • The percentage of positive tumor cells and expression level of Notch1 increased with higher histologic grade (r = 0.859, P < 0.05).
  • On the other hand, overexpression of Notch2 was detected in medulloblastoma (9/10) in contrast with lower expression of Notch1 (2/10).
  • CONCLUSIONS: Notch1 and Notch2 show differential expression in astrocytoma and medulloblastoma.
  • This may be related to their different functional activities during the process of brain development.
  • [MeSH-major] Astrocytoma / metabolism. Biomarkers, Tumor / metabolism. Medulloblastoma / metabolism. Receptor, Notch1 / metabolism. Receptor, Notch2 / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Brain / metabolism. Brain Neoplasms / metabolism. Child. Child, Preschool. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Young Adult

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  • (PMID = 19035115.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptor, Notch1; 0 / Receptor, Notch2
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15. Brandes AA, Franceschi E: Neuro-oncology: Genetic variation in pediatric and adult brain tumors. Nat Rev Neurol; 2010 Dec;6(12):653-4
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  • [Title] Neuro-oncology: Genetic variation in pediatric and adult brain tumors.
  • Two new studies suggest that pediatric medulloblastomas and high-grade gliomas are genetically different from the same tumors in adults.
  • Age-dependent gene expression might affect tumor biology; therefore, therapies for adult medulloblastomas or gliomas might not produce the same clinical outcomes in pediatric patients, and vice versa.
  • [MeSH-major] Brain Neoplasms / genetics. Cerebellar Neoplasms / genetics. Gene Expression Profiling. Glioma / genetics. Medulloblastoma / genetics
  • [MeSH-minor] Adult. Child. Genetic Variation. Humans

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  • (PMID = 21131914.001).
  • [ISSN] 1759-4766
  • [Journal-full-title] Nature reviews. Neurology
  • [ISO-abbreviation] Nat Rev Neurol
  • [Language] eng
  • [Publication-type] News
  • [Publication-country] England
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16. Spiller SE, Ravanpay AC, Hahn AW, Olson JM: Suberoylanilide hydroxamic acid is effective in preclinical studies of medulloblastoma. J Neurooncol; 2006 Sep;79(3):259-70
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  • [Title] Suberoylanilide hydroxamic acid is effective in preclinical studies of medulloblastoma.
  • PURPOSE: Suberoylanilide hydroxamic acid (SAHA) has been studied in adult solid and hematologic malignancies.
  • However, little information has been reported on the effects of SAHA on central nervous system (CNS) tumors including medulloblastoma, the most common malignant brain tumor in children.
  • We investigated SAHA in preclinical medulloblastoma models to determine its anti-cancer efficacy as well as its ability to affect intracranial lesions when administered systemically.
  • EXPERIMENTAL DESIGN AND RESULTS: Tissue culture studies were performed treating primary human fibroblasts, established medulloblastoma cell lines, and primary human medulloblastoma tumors with SAHA.
  • At 10 microM concentration, SAHA had little effect on normal fibroblasts but caused >90% apoptosis in cultured medulloblastoma cells.
  • Primary medulloblastomas from patients were sensitive to SAHA compared to vehicle alone in ex vivo studies.
  • In athymic mice with medulloblastoma xenograft tumors, oral SAHA resulted in apoptosis of tumor tissue and significantly slowed tumor growth.
  • In the ND2:Smo transgenic mouse medulloblastoma model, SAHA treatment caused significant apoptosis in these cerebellar tumors.
  • CONCLUSIONS: SAHA effectively induces cell death in established medulloblastoma cell lines, human patient primary tumor cultures, medulloblastoma xenografts and intracranial spontaneous medulloblastomas.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cerebellar Neoplasms / drug therapy. Hydroxamic Acids / pharmacology. Medulloblastoma / drug therapy

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  • (PMID = 16645722.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA112350-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hydroxamic Acids; 58IFB293JI / vorinostat
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17. Chang Q, Ng HK: [Different hypermethylation status of RASSF1A in medulloblastoma and supratentorial primitive neuroectodermal tumor]. Zhonghua Bing Li Xue Za Zhi; 2007 Jan;36(1):24-8
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  • [Title] [Different hypermethylation status of RASSF1A in medulloblastoma and supratentorial primitive neuroectodermal tumor].
  • OBJECTIVE: To investigate the epigenetic involvement of RASSF1A in intracranial primitive neuroectodermal tumors (PNETs) and compare the methylation patterns between medulloblastoma (MBs) and supratentorial PNETs (SPNETs).
  • These results demonstrated that such epigenetic alteration was tumor-specific.
  • [MeSH-major] Brain Neoplasms / genetics. Cerebellar Neoplasms / genetics. Medulloblastoma / genetics. Neuroectodermal Tumors, Primitive / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Line, Tumor. Child. Child, Preschool. DNA Methylation. Female. Gene Expression Regulation, Neoplastic. Gene Silencing. HeLa Cells. Humans. Infant. Male. Promoter Regions, Genetic / genetics. Reverse Transcriptase Polymerase Chain Reaction. Young Adult


18. Korshunov A, Benner A, Remke M, Lichter P, von Deimling A, Pfister S: Accumulation of genomic aberrations during clinical progression of medulloblastoma. Acta Neuropathol; 2008 Oct;116(4):383-90
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  • [Title] Accumulation of genomic aberrations during clinical progression of medulloblastoma.
  • Medulloblastomas comprise the most frequent malignant brain tumor in childhood and one of the biggest challenges in pediatric oncology.
  • The current concept suggests that these tumors may undergo stepwise progression as it has been shown for other brain tumors.
  • However, conclusive evidence of molecular progression over time has not been demonstrated yet for medulloblastoma.
  • In the present study, 28 pairs of medulloblastoma at primary diagnosis and at the time of recurrence, either occurring as local tumor regrowth or tumor dissemination, were histopathologically and molecularly analyzed.
  • These results suggest that early recurrence in medulloblastoma mainly occurs in tumors with a highly malignant genotype and phenotype per se, whereas late recurrence is often dependent on tumor evolution toward a more malignant biology.
  • Therefore, biopsy of recurrent tumors should be performed to assess the biologic properties of the relapsed tumor, especially when targeted therapy approaches are considered.
  • [MeSH-major] Cerebellar Neoplasms / genetics. Chromosome Aberrations. Chromosomes, Human, Pair 17 / genetics. Chromosomes, Human, Pair 6 / genetics. Medulloblastoma / genetics. Nuclear Proteins / genetics. Oncogene Proteins / genetics. Proto-Oncogene Proteins c-myc / genetics
  • [MeSH-minor] Adolescent. Adult. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Child. Child, Preschool. Cytogenetic Analysis. Disease Progression. Female. Humans. Male. Neoplasm Recurrence, Local / genetics. Prognosis

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  • (PMID = 18704466.001).
  • [ISSN] 1432-0533
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MYC protein, human; 0 / MYCN protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins; 0 / Proto-Oncogene Proteins c-myc
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19. Tabori U, Sung L, Hukin J, Laperriere N, Crooks B, Carret AS, Silva M, Odame I, Mpofu C, Strother D, Wilson B, Samson Y, Bouffet E, Canadian Pediatric Brain Tumor Consortium: Distinctive clinical course and pattern of relapse in adolescents with medulloblastoma. Int J Radiat Oncol Biol Phys; 2006 Feb 1;64(2):402-7
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  • [Title] Distinctive clinical course and pattern of relapse in adolescents with medulloblastoma.
  • PURPOSE: To report the clinical course of adolescents with medulloblastoma, with specific emphasis on prognosis and pattern of relapse.
  • METHODS AND MATERIALS: We retrospectively studied the clinical course and outcomes of children aged 10-20 years with medulloblastoma, treated at centers throughout Canada between 1986 and 2003.
  • CONCLUSIONS: Our study suggests that adolescents with medulloblastoma might have a unique prognosis and pattern of relapse, dissimilar to those in younger children.
  • [MeSH-major] Cerebellar Neoplasms / mortality. Medulloblastoma / mortality. Neoplasm Recurrence, Local / mortality
  • [MeSH-minor] Adolescent. Adult. Age Factors. Analysis of Variance. Child. Disease-Free Survival. Female. Humans. Male. Prognosis. Recurrence. Retrospective Studies. Sex Factors

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  • (PMID = 16198067.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
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20. Rushing EJ, Smith AB, Smirniotopoulos JG, Douglas AF, Zeng W, Azumi N: Occult leptomeningeal large cell medulloblastoma in an adult. Clin Neuropathol; 2009 May-Jun;28(3):188-92
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  • [Title] Occult leptomeningeal large cell medulloblastoma in an adult.
  • OBJECTIVE AND IMPORTANCE: Large cell medulloblastoma is an uncommon malignancy of childhood that often pursues an aggressive clinical course.
  • We report the first case of this entity in an adult that proved to be an unsuspected primary leptomeningeal tumor.
  • Postmortem examination of the brain was notable for necrotic cerebellar tonsils, but demonstrated no evidence of an intraparenchymal mass lesion.
  • Microscopic examination of the cerebellum revealed discohesive neoplastic cells, which showed characteristic dot-like immunoreactivity for synaptophysin, diagnostic of large cell medulloblastoma within the subarachnoid space.
  • [MeSH-major] Cerebellar Neoplasms / pathology. Medulloblastoma / pathology. Meningeal Neoplasms / pathology
  • [MeSH-minor] Adult. Arnold-Chiari Malformation / complications. Fatal Outcome. Humans. Intervertebral Disc Displacement / complications. Magnetic Resonance Imaging. Male

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  • (PMID = 19537136.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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21. Scott DK, Straughton D, Cole M, Bailey S, Ellison DW, Clifford SC: Identification and analysis of tumor suppressor loci at chromosome 10q23.3-10q25.3 in medulloblastoma. Cell Cycle; 2006 Oct;5(20):2381-9
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  • [Title] Identification and analysis of tumor suppressor loci at chromosome 10q23.3-10q25.3 in medulloblastoma.
  • Abnormalities of chromosome 10 are frequently observed in the development of medulloblastoma, the most common malignant brain tumor of childhood.
  • This region contains three genes, MXI1, SUFU and BTRC, which represent putative medulloblastoma tumor suppressor (TS) genes on the basis of either (i) negative regulation of critical medulloblastoma pathways, or (ii) mutation in other cancer types.
  • A MXI1 mutation was identified which abolishes its translation initiation site (A1G; MET1VAL), however no further tumor-specific sequence variations were detected.
  • These findings implicate the inactivation of critical TS loci at 10q23.3-25.3 in medulloblastoma, however comprehensive analysis of SUFU, BTRC and MXI1 indicates they are unlikely to represent major targets of these allelic losses.
  • MXI1 mutation appears to play a role in the pathogenesis of a small subset of cases, and suggests an alternative mechanism to MYC amplification for disruption of the MYC/MAD/MAX network in medulloblastoma.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. Chromosomes, Human, Pair 10. Genes, Tumor Suppressor. Medulloblastoma / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. DNA Mutational Analysis. Female. Gene Silencing. Humans. Infant. Male. Physical Chromosome Mapping. Repressor Proteins / genetics. beta-Transducin Repeat-Containing Proteins / genetics

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  • (PMID = 17102621.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BTRC protein, human; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / MXI1 protein, human; 0 / Repressor Proteins; 0 / SUFU protein, human; 0 / Tumor Suppressor Proteins; 0 / beta-Transducin Repeat-Containing Proteins
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22. Germanwala AV, Mai JC, Tomycz ND, Niranjan A, Flickinger JC, Kondziolka D, Lunsford LD: Boost Gamma Knife surgery during multimodality management of adult medulloblastoma. J Neurosurg; 2008 Feb;108(2):204-9
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  • [Title] Boost Gamma Knife surgery during multimodality management of adult medulloblastoma.
  • OBJECT: The aim of this paper was to determine prognostic factors for adult medulloblastoma treated with boost Gamma Knife surgery (GKS) following resection and craniospinal irradiation.
  • METHODS: The authors performed a retrospective analysis of 12 adult patients with histologically proven medulloblastoma or supratentorial primitive neuroectodermal tumor who between February 1991 and December 2004 underwent >or=1 sessions of GKS for posttreatment residual or recurrent tumors (6 tumors in each group).
  • Stereotactic radiosurgery was applied to residual and recurrent posterior fossa tumor as well as to foci of intracranial medulloblastoma metastases.
  • The mean GKS-treated tumor volume was 9.4 cm3 (range 0.5-39 cm3).
  • RESULTS: Following adjunctive radiosurgery, 5 patients had no evidence of tumor on magnetic resonance (MR) imaging, 3 patients had stable tumor burden on MR imaging, and 4 patients had evidence of tumor progression locally with or without intracranial metastases.
  • All patients with tumor progression died.
  • The majority of patients who achieved tumor eradication (80%) and tumor stabilization (67%) after GKS had residual tumor as the reason for their referral for GKS.
  • The best outcomes were attained in patients with residual disease who were younger, had smaller tumor volumes, had no evidence of metastatic disease, and had received higher cumulative GKS doses.
  • CONCLUSIONS: Single or multiple GKS sessions were a well-tolerated, feasible, and effective adjunctive treatment for posterior fossa residual or recurrent medulloblastoma as well as intracranial metastatic medulloblastoma in adult patients.
  • [MeSH-major] Cerebellar Neoplasms / surgery. Medulloblastoma / surgery. Neoadjuvant Therapy. Radiosurgery / methods
  • [MeSH-minor] Adult. Age Factors. Chemotherapy, Adjuvant. Cranial Irradiation. Disease Progression. Female. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Recurrence, Local / radiotherapy. Neoplasm Recurrence, Local / surgery. Neoplasm, Residual. Neuroectodermal Tumors / radiotherapy. Neuroectodermal Tumors / surgery. Remission Induction. Retrospective Studies. Spine / radiation effects. Supratentorial Neoplasms / radiotherapy. Supratentorial Neoplasms / surgery. Survival Rate. Time Factors. Treatment Outcome

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  • (PMID = 18240913.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Zawlik I, Zakrzewska M, Witusik M, Golanska E, Kulczycka-Wojdala D, Szybka M, Piaskowski S, Wozniak K, Zakrzewski K, Papierz W, Liberski PP, Rieske P: KCTD11 expression in medulloblastoma is lower than in adult cerebellum and higher than in neural stem cells. Cancer Genet Cytogenet; 2006 Oct 1;170(1):24-8
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  • [Title] KCTD11 expression in medulloblastoma is lower than in adult cerebellum and higher than in neural stem cells.
  • Medulloblastoma (MB) is the most common malignant brain tumor of childhood, and the most frequent associated genetic alteration is loss of heterozygosity on chromosome region 7p13.
  • We used real-time polymerase chain reaction in 20 tissue samples of primary MB to examine the transcriptional level of the two genes, with reference to two types of controls: adult cerebellum and fetal neural stem cells.
  • A significant reduction of KCTD11 expression relative to adult normal cerebellum was detected in 14 of 20 (70%) of MB samples.
  • HIC1 gene expression was low ( approximately 100 times lower than KCTD11 expression) in MB, and low also in both adult cerebellum and neural stem cells.
  • Hypermethylation of the 5'UTR or the central region of HIC1 (or both) was detected in a significant number of MB samples, as well as in cerebellum and neural stem cells.
  • Our data suggest that KCTD11 may play an important role in MB tumorigenesis, but do not support the role of HIC1 in this tumor development.
  • [MeSH-major] Cerebellum / metabolism. Medulloblastoma / genetics. Nervous System / metabolism. Potassium Channels / genetics. Stem Cells / metabolism

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  • (PMID = 16965951.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / HIC1 protein, human; 0 / KCTD11 protein, human; 0 / Kruppel-Like Transcription Factors; 0 / Potassium Channels; 0 / Transcription Factors
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24. Siu IM, Bai R, Gallia GL, Edwards JB, Tyler BM, Eberhart CG, Riggins GJ: Coexpression of neuronatin splice forms promotes medulloblastoma growth. Neuro Oncol; 2008 Oct;10(5):716-24
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  • [Title] Coexpression of neuronatin splice forms promotes medulloblastoma growth.
  • Medulloblastoma (MB) is the most common pediatric brain cancer.

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  • (PMID = 18701710.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS052507-02; United States / NINDS NIH HHS / NS / R01 NS052507; United States / NINDS NIH HHS / NS / NS052507; United States / NINDS NIH HHS / NS / R01 NS052507-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Membrane Proteins; 0 / NNAT protein, human; 0 / Nerve Tissue Proteins; 0 / Protein Isoforms
  • [Other-IDs] NLM/ PMC2666248
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25. Massimino M, Gandola L, Collini P, Seregni E, Marchianò A, Serra A, Pignoli E, Spreafico F, Pallotti F, Terenziani M, Biassoni V, Bombardieri E, Fossati-Bellani F: Thyroid-stimulating hormone suppression for protection against hypothyroidism due to craniospinal irradiation for childhood medulloblastoma/primitive neuroectodermal tumor. Int J Radiat Oncol Biol Phys; 2007 Oct 1;69(2):404-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Thyroid-stimulating hormone suppression for protection against hypothyroidism due to craniospinal irradiation for childhood medulloblastoma/primitive neuroectodermal tumor.
  • Hence, our study was launched in 1998 to evaluate the protective effect of TSH suppression during CSI for medulloblastoma/primitive neuroectodermal tumor.
  • PATIENTS AND METHODS: From Jan 1998 to Feb 2001, a total of 37 euthyroid children scheduled for CSI for medulloblastoma/primitive neuroectodermal tumor underwent thyroid ultrasound and free triiodothyronine (FT3), free thyroxine (FT4), and TSH evaluation at the beginning and end of CSI.
  • [MeSH-major] Brain Neoplasms / radiotherapy. Cranial Irradiation / adverse effects. Hypothyroidism / prevention & control. Medulloblastoma / radiotherapy. Neuroectodermal Tumors, Primitive / radiotherapy. Thyrotropin / antagonists & inhibitors
  • [MeSH-minor] Adolescent. Adult. Biomarkers / blood. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Radiotherapy Dosage. Thyroxine / blood. Triiodothyronine / blood


26. Shim KW, Joo SY, Kim SH, Choi JU, Kim DS: Prediction of prognosis in children with medulloblastoma by using immunohistochemical analysis and tissue microarray. J Neurosurg Pediatr; 2008 Mar;1(3):196-205
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prediction of prognosis in children with medulloblastoma by using immunohistochemical analysis and tissue microarray.
  • OBJECTIVES: Medulloblastoma is the most common malignant neuroepithelial tumor found in children.
  • Several reports have described efforts to identify the prognostic significance of various patterns of pathological and immunohistochemical features in medulloblastoma, but the published data appear to be controversial.
  • The authors therefore attempted to demonstrate these prognostic factors convincingly in a retrospective study performed in patients with medulloblastoma.
  • METHODS: The data used were obtained in 58 patients with medulloblastoma who were > 3 years of age and in whom > 1 year of follow-up was available after the maximal resection, craniospinal irradiation, and chemotherapy treatments.
  • In addition, the authors tried to determine the prognostic utility of these results in this tumor category.
  • RESULTS: There was no statistically significant correlation between the prognosis and the degree of cell differentiation, but a positive correlation was noted between the PI and the AI in a tumor mass.
  • The number of cases with a PI > 10% was significantly greater in the group of tumors in patients with recurrent medulloblastoma.
  • Most importantly, the PI is the only significant prognostic factor for the overall survival of patients with medulloblastoma.
  • CONCLUSIONS: Therefore, the authors suggest that the PI is directly linked to the prognostic factor for medulloblastoma and that immunohistochemical staining is a potentially powerful tool for predicting the prognosis of patients with medulloblastoma.
  • [MeSH-major] Biomarkers, Tumor / analysis. Cerebellar Neoplasms / pathology. Medulloblastoma / pathology
  • [MeSH-minor] Adolescent. Adult. Apoptosis / physiology. Cell Differentiation / physiology. Cell Proliferation. Chemotherapy, Adjuvant. Child. Child, Preschool. Female. Follow-Up Studies. Forecasting. Humans. Immunohistochemistry. Male. Microarray Analysis. Neoadjuvant Therapy. Neoplasm Recurrence, Local / pathology. Prognosis. Radiotherapy, Adjuvant. Receptor, ErbB-3 / analysis. Receptor, trkC / analysis. Retrospective Studies. Treatment Outcome


27. Hoffman S, Schellinger KA, Propp JM, McCarthy BJ, Campbell RT, Davis FG: Seasonal variation in incidence of pediatric medulloblastoma in the United States, 1995-2001. Neuroepidemiology; 2007;29(1-2):89-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Seasonal variation in incidence of pediatric medulloblastoma in the United States, 1995-2001.
  • BACKGROUND/AIMS: Brain tumors are the second most common pediatric malignancy.
  • The literature suggests that one of the most common subtypes of malignant childhood brain tumor, medulloblastoma, has some seasonal variation in incidence by month of birth.
  • METHODS: Data from cases in the Central Brain Tumor Registry of the United States, including primary brain tumor cases diagnosed in children (0-19 years) between the years 1995 and 2001 from 13 state cancer registries, were analyzed to determine whether there was seasonal variation.
  • RESULTS: Seasonal variation in incidence by month of birth was highly statistically significant for medulloblastoma, not otherwise specified (NOS) (p = 0.016), with the peak occurring in October.
  • Medulloblastoma, NOS also demonstrated seasonal variation in incidence by month of birth in children aged 5-19 (p = 0.041), especially females aged 5-19 (p = 0.034), with the peak in October.
  • There were no significant results for brain tumors overall, or for the other most common pediatric tumor subtypes (pilocytic astrocytoma, other astrocytoma, and ependymoma).
  • CONCLUSION: These preliminary results indicate seasonal variation unique to medulloblastoma incidence by month of birth and may provide evidence for an environmental exposure etiology, though further studies are needed to explore specific hypotheses.
  • [MeSH-major] Cerebellar Neoplasms / epidemiology. Medulloblastoma / epidemiology. Parturition. Seasons
  • [MeSH-minor] Adolescent. Adult. Birth Rate. Child. Child, Preschool. Female. Humans. Incidence. Male. Registries. United States / epidemiology

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  • [Copyright] (c) 2007 S. Karger AG, Basel.
  • (PMID = 17925600.001).
  • [ISSN] 1423-0208
  • [Journal-full-title] Neuroepidemiology
  • [ISO-abbreviation] Neuroepidemiology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
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28. Rudin CM, Hann CL, Laterra J, Yauch RL, Callahan CA, Fu L, Holcomb T, Stinson J, Gould SE, Coleman B, LoRusso PM, Von Hoff DD, de Sauvage FJ, Low JA: Treatment of medulloblastoma with hedgehog pathway inhibitor GDC-0449. N Engl J Med; 2009 Sep 17;361(12):1173-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of medulloblastoma with hedgehog pathway inhibitor GDC-0449.
  • Medulloblastoma is the most common malignant brain tumor in children.
  • Aberrant activation of the hedgehog signaling pathway is strongly implicated in the development of some cases of medulloblastoma.
  • A 26-year-old man with metastatic medulloblastoma that was refractory to multiple therapies was treated with a novel hedgehog pathway inhibitor, GDC-0449; treatment resulted in rapid (although transient) regression of the tumor and reduction of symptoms.
  • Molecular analyses of tumor specimens obtained before treatment suggested that there was activation of the hedgehog pathway, with loss of heterozygosity and somatic mutation of the gene encoding patched homologue 1 (PTCH1), a key negative regulator of hedgehog signaling.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Benzimidazoles / therapeutic use. Cerebellar Neoplasms / drug therapy. Hedgehog Proteins / antagonists & inhibitors. Medulloblastoma / drug therapy
  • [MeSH-minor] Adult. Anilides. Gene Expression. Humans. Male. Patched Receptors. Patched-1 Receptor. Polymerase Chain Reaction. Pyridines. RNA, Messenger / metabolism. Receptors, Cell Surface / genetics. Receptors, Cell Surface / metabolism. Signal Transduction / drug effects. Transcription Factors / genetics. Transcription Factors / metabolism. Zinc Finger Protein GLI1


29. Pierson J, Hostager B, Fan R, Vibhakar R: Regulation of cyclin dependent kinase 6 by microRNA 124 in medulloblastoma. J Neurooncol; 2008 Oct;90(1):1-7
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  • [Title] Regulation of cyclin dependent kinase 6 by microRNA 124 in medulloblastoma.
  • Despite recent advances in treatment medulloblastoma continues to remain a vexing problem.
  • Recently increased expression of cyclin dependent kinase 6 (CDK6) was identified as an adverse prognostic marker in medulloblastoma.
  • We hypothesized that CDK6 expression is also regulated by microRNAs in medulloblastoma.
  • We identified putative miR sites in the CDK6 including microRNA 124a, a brain enriched microRNA.
  • Expression of miR 124a was significantly decreased in medulloblastoma cells compared to normal adult cerebellum.
  • Functional association between miR 124a and CDK6 in medulloblastoma was established using luciferase assays.
  • Additionally, re-expression of miR 124a in medulloblastoma cells decreased expression of CDK6 protein.
  • Transfection of miR 124 significantly decreases medulloblastoma cell growth but does not alter apoptosis.
  • Our data strongly indicate that CDK6 is regulated by microRNA 124 in medulloblastoma and that miR 124 modulates medulloblastoma cell growth.
  • [MeSH-major] Brain Neoplasms / genetics. Cyclin-Dependent Kinase 6 / genetics. Gene Expression Regulation, Neoplastic. Medulloblastoma / genetics. MicroRNAs / genetics
  • [MeSH-minor] Apoptosis / physiology. Base Sequence. Blotting, Western. Cell Line, Tumor. Cell Proliferation. Humans. Molecular Sequence Data. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18607543.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / RNA, Messenger; EC 2.7.11.22 / Cyclin-Dependent Kinase 6
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30. Shu XH, Li H, Sun Z, Wu ML, Ma JX, Wang JM, Wang Q, Sun Y, Fu YS, Chen XY, Kong QY, Liu J: Identification of metabolic pattern and bioactive form of resveratrol in human medulloblastoma cells. Biochem Pharmacol; 2010 May 15;79(10):1516-25
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  • [Title] Identification of metabolic pattern and bioactive form of resveratrol in human medulloblastoma cells.
  • This issue was addressed here by identifying the metabolic pattern and the bioactive form of resveratrol in a resveratrol-sensitive human medulloblastoma cell line, UW228-3.
  • The cell lysates and condition media of UW228-3 cells with or without 100 microM resveratrol treatment were analyzed by HPLC and LC/MS which revealed (1) that resveratrol was chemically unstable and the spontaneous generation of cis-resveratrol reduced resveratrol's anti-medulloblastoma efficacy and (2) that resveratrol monosulfate was the major metabolite of the cells.
  • To identify the bioactive form of resveratrol, a mixture-containing approximately half fraction of resveratrol monosulfate was prepared by incubating trans-resveratrol with freshly prepared rat brain lysates.
  • Medulloblastoma cells treated by 100 microM of this mixture showed attenuated cell crisis.
  • The overall levels of the three brain-associated sulfotransferases (SULT1A1, 1C2 and 4A1) were low in medulloblastoma cells in vivo and in vitro in comparison with that in human noncancerous and rat normal cerebella; resveratrol could more or less up-regulate the production of these enzymes in UW228-3 cells but their overall level was still lower than that in normal cerebellum tissue.
  • Our study thus demonstrated for the first time that trans-resveratrol is the bioactive form in medulloblastoma cells in which the expression of brain-associated SULTs was down-regulated, resulting in the increased intracellular bioavailability and anti-medulloblastoma efficacy of trans-resveratrol.
  • [MeSH-major] Antineoplastic Agents / metabolism. Antineoplastic Agents / pharmacokinetics. Cerebellar Neoplasms / drug therapy. Medulloblastoma / drug therapy. Stilbenes / pharmacokinetics
  • [MeSH-minor] Adolescent. Animals. Biotransformation. Blotting, Western. Cell Line, Tumor. Child. Chromatography, High Pressure Liquid. Humans. Rats. Reverse Transcriptase Polymerase Chain Reaction. Sulfotransferases / metabolism. Young Adult

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20105429.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Stilbenes; EC 2.8.2.- / Sulfotransferases; Q369O8926L / resveratrol
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31. Roland JT Jr, Cosetti M, Liebman T, Waltzman S, Allen JC: Cochlear implantation following treatment for medulloblastoma. Laryngoscope; 2010 Jan;120(1):139-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cochlear implantation following treatment for medulloblastoma.
  • OBJECTIVES/HYPOTHESIS: Medulloblastoma is the most common pediatric malignant tumor of the central nervous system in children.
  • Issues of CI in this population, including diagnosis, treatment of preoperative middle ear disease, operative and postoperative course, performance data, and long-term tumor surveillance are highlighted and reviewed.
  • METHODS: Three patients treated for pediatric medulloblastoma with surgical resection, postoperative hyperfractioned craniospinal radiotherapy, and multiagent adjuvant chemotherapy who underwent cochlear implantation were identified.
  • CONCLUSIONS: Patients treated for pediatric medulloblastoma develop otologic sequelae, including profound SNHL, and may require cochlear implantation.
  • [MeSH-major] Brain Neoplasms / therapy. Cochlear Implantation. Hearing Loss, Sensorineural / surgery. Medulloblastoma / therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Combined Modality Therapy. Humans. Retrospective Studies. Treatment Outcome


32. Zitterbart K, Zavrelova I, Kadlecova J, Spesna R, Kratochvilova A, Pavelka Z, Sterba J: p73 expression in medulloblastoma: TAp73/DeltaNp73 transcript detection and possible association of p73alpha/DeltaNp73 immunoreactivity with survival. Acta Neuropathol; 2007 Dec;114(6):641-50
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  • [Title] p73 expression in medulloblastoma: TAp73/DeltaNp73 transcript detection and possible association of p73alpha/DeltaNp73 immunoreactivity with survival.
  • Recently, several TP73 transcripts have been revealed in medulloblastoma (MB), the most common malignant brain tumor in children.
  • We report significant differences for TAp73 and DeltaNp73 mRNA expression between tumor tissues and reference (P = 0.013, P = 0.028).
  • In normal cerebellum, positive staining for p73alpha and DeltaNp73 was observed in the Purkinje cells of newborns, not adult samples, which supports the developmental role of TP73 during organogenesis of the human cerebellum.
  • Our results indicate the involvement of p73 protein in MB tumorigenesis and define TP73 as a potential prognostic and therapeutic target for medulloblastoma.
  • [MeSH-major] Brain Neoplasms / metabolism. DNA-Binding Proteins / metabolism. Medulloblastoma / metabolism. Nuclear Proteins / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Biomarkers, Tumor / analysis. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Brain / metabolism. Brain / pathology. Brain / physiopathology. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Child. Child, Preschool. Female. Gene Expression Regulation, Neoplastic / genetics. Humans. Immunohistochemistry. Male. Prognosis. Protein Isoforms / genetics. Protein Isoforms / isolation & purification. Protein Isoforms / metabolism. RNA, Messenger / analysis. RNA, Messenger / metabolism. Retrospective Studies. Survival Rate

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  • [ErratumIn] Acta Neuropathol. 2008 Nov;116(5):579-80
  • (PMID = 17912537.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins
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33. Mühlisch J, Bajanowski T, Rickert CH, Roggendorf W, Würthwein G, Jürgens H, Frühwald MC: Frequent but borderline methylation of p16 (INK4a) and TIMP3 in medulloblastoma and sPNET revealed by quantitative analyses. J Neurooncol; 2007 May;83(1):17-29
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  • [Title] Frequent but borderline methylation of p16 (INK4a) and TIMP3 in medulloblastoma and sPNET revealed by quantitative analyses.
  • Certain risk groups among tumors of the central nervous system (CNS) in children take an almost inevitably fatal course.
  • Aberrant methylation is common in malignant brain tumors of childhood and may have implications for stratification and therapy.
  • Methylation of p16 (INK4A), p14 (ARF), TIMP3, CDH1, p15 (INK4B )and DAPK1 in medulloblastoma (MB) and ependymoma has been discussed controversially in the literature.
  • Only p16 (INK4A )and TIMP3 were methylated consistently in medulloblastomas (p16 (INK4A ) 14%, TIMP3 11%) and p16 (INK4A) also in anaplastic ependymomas (1/4 tumors).
  • Therapeutic and diagnostic implications urge into depth analyses of methylation as a mechanism, which might fill some of the gaps of our understanding of brain tumor origin.
  • [MeSH-major] Brain Neoplasms / genetics. Cerebellar Neoplasms / genetics. DNA Methylation. Genes, p16. Medulloblastoma / genetics. Neuroectodermal Tumors, Primitive / genetics. Tissue Inhibitor of Metalloproteinase-3 / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Apoptosis Regulatory Proteins / genetics. Calcium-Calmodulin-Dependent Protein Kinases / genetics. Child. Child, Preschool. Death-Associated Protein Kinases. Female. Gene Silencing. Humans. Infant. Male. Middle Aged. Nerve Tissue Proteins / genetics. Receptors, Immunologic / genetics

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  • (PMID = 17206475.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Nerve Tissue Proteins; 0 / Receptors, Immunologic; 0 / TIMP3 protein, human; 0 / Tissue Inhibitor of Metalloproteinase-3; 0 / roundabout protein; EC 2.7.11.1 / DAPK1 protein, human; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
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34. Teglund S, Toftgård R: Hedgehog beyond medulloblastoma and basal cell carcinoma. Biochim Biophys Acta; 2010 Apr;1805(2):181-208
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  • [Title] Hedgehog beyond medulloblastoma and basal cell carcinoma.
  • The Hedgehog (Hh) signaling pathway is of central importance during embryo development in metazoans and governs a diverse array of processes including cell proliferation, differentiation, and tissue patterning.
  • In normal adult physiology, the pathway is implicated in stem cell maintenance, tissue repair and regeneration.
  • The Hh pathway is firmly linked to the etiology of basal cell carcinoma and to at least a subset of medulloblastoma.
  • In this review, we provide an overview of the pathway's role in various tumor types, where much of the framework for Hh-dependent malignancies has been elucidated in experimental mouse models.
  • [MeSH-major] Brain Neoplasms / metabolism. Carcinoma, Basal Cell / metabolism. Hedgehog Proteins / metabolism. Medulloblastoma / metabolism. Signal Transduction / physiology. Skin Neoplasms / metabolism


35. Yang LS, Wang YQ, Huang FP: [Correlation between the prognosis of medulloblastoma and relevant clinical factors: analysis of 73 cases]. Zhonghua Yi Xue Za Zhi; 2007 May 22;87(19):1322-5
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  • [Title] [Correlation between the prognosis of medulloblastoma and relevant clinical factors: analysis of 73 cases].
  • OBJECTIVE: To analyze the correlation between the prognosis of medulloblastoma (MB) and relevant clinical factors.
  • The correlation between the prognosis and the clinical factors, such and sex, age, tumor location, extent of tumor resection, brainstem invasion, radiotherapy, chemotherapy, ventriculoperitoneal shunt and glial differentiation was analyzed.
  • Those undergoing whole brain/posterior fossa plus spinal axis radiotherapy showed a better prognosis than those undergoing whole brain/posterior fossa radiotherapy.
  • [MeSH-major] Central Nervous System Neoplasms / therapy. Medulloblastoma / therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Combined Modality Therapy. Female. Follow-Up Studies. Humans. Kaplan-Meier Estimate. Male. Prognosis. Retrospective Studies. Survival Rate

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  • (PMID = 17727776.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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36. Wolff JE, Hüttermann U, Askins MA: Quantifying health status outcomes in pediatric medulloblastoma patients. Anticancer Res; 2007 Jan-Feb;27(1B):523-9
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  • [Title] Quantifying health status outcomes in pediatric medulloblastoma patients.
  • BACKGROUND: Comprehensive, efficient health status assessment tools are needed for multi-center studies examining childhood brain tumor treatment outcomes.
  • PATIENTS AND METHODS: The FMH was compared with the medical assessments, intelligence scores, and behavioral/emotional adjustment scores of 21 survivors of medulloblastoma to examine the instrument's feasibility and discriminate validity.
  • CONCLUSION: The FMH is useful as an objective, easily administered measure of health status in brain tumor patients.
  • [MeSH-major] Cerebellar Neoplasms / therapy. Health Status. Medulloblastoma / therapy. Outcome Assessment (Health Care) / methods. Surveys and Questionnaires
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Humans. Infant. Reproducibility of Results

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  • (PMID = 17348436.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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37. Massimino M, Gandola L, Spreafico F, Biassoni V, Luksch R, Collini P, Solero CN, Simonetti F, Pignoli E, Cefalo G, Poggi G, Modena P, Mariani L, Potepan P, Podda M, Casanova M, Pecori E, Acerno S, Ferrari A, Terenziani M, Meazza C, Polastri D, Ravagnani F, Fossati-Bellani F: No salvage using high-dose chemotherapy plus/minus reirradiation for relapsing previously irradiated medulloblastoma. Int J Radiat Oncol Biol Phys; 2009 Apr 1;73(5):1358-63
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  • [Title] No salvage using high-dose chemotherapy plus/minus reirradiation for relapsing previously irradiated medulloblastoma.
  • PURPOSE: Myeloablative regimens were frequently used for medulloblastoma relapsing after craniospinal irradiation (CSI): in 1997-2002, we used repeated surgery, standard-dose and myeloablative chemotherapy, and reirradiation.
  • RESULTS: Seventeen patients were treated: previous treatment included CSI of 19.5-36 Gy with posterior fossa/tumor boost and chemotherapy in 16 patients.
  • Relapse sites included leptomeninges in 9 patients, spine in 4 patients, posterior fossa in 3 patients, and brain in 1 patient.
  • Twelve of 14 patients with assessable tumor had an objective response after reinduction; 2 experienced progression and were not given the myeloablative courses.
  • A salvage therapy for medulloblastoma after CSI still needs to be sought.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cerebellar Neoplasms. Medulloblastoma. Neoplasm Recurrence, Local. Salvage Therapy
  • [MeSH-minor] Adolescent. Carboplatin / administration & dosage. Carboplatin / adverse effects. Child. Child, Preschool. Cisplatin / administration & dosage. Cisplatin / adverse effects. Combined Modality Therapy / methods. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Disease-Free Survival. Drug Administration Schedule. Etoposide / administration & dosage. Etoposide / adverse effects. Female. Granulocyte Colony-Stimulating Factor / administration & dosage. Humans. Male. Methotrexate / administration & dosage. Methotrexate / adverse effects. Radiotherapy Dosage. Remission Induction / methods. Thiotepa / administration & dosage. Thiotepa / adverse effects. Vincristine / administration & dosage. Vincristine / adverse effects. Young Adult

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  • (PMID = 19019566.001).
  • [ISSN] 1879-355X
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; 905Z5W3GKH / Thiotepa; BG3F62OND5 / Carboplatin; Q20Q21Q62J / Cisplatin; YL5FZ2Y5U1 / Methotrexate
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38. Lueth M, von Deimling A, Pietsch T, Wong LJ, Kurtz A, Henze G, Driever PH: Medulloblastoma harbor somatic mitochondrial DNA mutations in the D-loop region. J Pediatr Hematol Oncol; 2010 Mar;32(2):156-9
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  • [Title] Medulloblastoma harbor somatic mitochondrial DNA mutations in the D-loop region.
  • Despite the growing knowledge on molecular risk factors of the most common malignant brain tumor in childhood, medulloblastoma, its biology remains only partially understood.
  • A previous study investigating the entire mitochondrial genome of medulloblastoma revealed a number of somatic mutations in tumor and corresponding cerebrospinal fluid samples.
  • In our present study we sought to corroborate these results on somatic and germ line mutations by comparing the complete mitochondrial genome sequences of medulloblastoma tissue in a further cohort of patients.
  • Analysis of the entire mitochondrial genome by temporal temperature gel electrophoresis and direct sequencing revealed 6 somatic mutations in 6 of 15 medulloblastoma.
  • These results are in support of our previous findings on frequency of somatic mitochondrial mutations in medulloblastoma.
  • [MeSH-major] Cerebellar Neoplasms / genetics. DNA, Mitochondrial / genetics. Medulloblastoma / genetics. Mutation
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Genome, Mitochondrial. Humans. Infant. Male

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  • (PMID = 20147852.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Mitochondrial
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39. Kadota RP, Mahoney DH, Doyle J, Duerst R, Friedman H, Holmes E, Kun L, Zhou T, Pollack IF: Dose intensive melphalan and cyclophosphamide with autologous hematopoietic stem cells for recurrent medulloblastoma or germinoma. Pediatr Blood Cancer; 2008 Nov;51(5):675-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dose intensive melphalan and cyclophosphamide with autologous hematopoietic stem cells for recurrent medulloblastoma or germinoma.
  • PURPOSE: To determine the response, toxicity, and survival for children with progressive or recurrent medulloblastoma and germinoma using a single myeloablative course of chemotherapy supported by autologous hematopoietic stem cells.
  • There were 6 medulloblastoma and 3 germinoma survivors with a median follow-up of 7.5 years (range = 2.8-10).
  • CONCLUSION: Myeloablative chemotherapy consisting of cyclophosphamide and melphalan was tolerable in the relapsed brain tumor setting with 19/29 cases achieving CR or CCR status and 9/29 becoming long-term survivors.

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
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  • (PMID = 18623206.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA098543-06; United States / NCI NIH HHS / CA / CA98543; United States / NCI NIH HHS / CA / U10 CA098413-06; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U10 CA098543; None / None / / U10 CA098413-06; None / None / / U10 CA098543-06
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 8N3DW7272P / Cyclophosphamide; Q41OR9510P / Melphalan
  • [Other-IDs] NLM/ NIHMS123029; NLM/ PMC2900925
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40. Oba-Shinjo SM, Caballero OL, Jungbluth AA, Rosemberg S, Old LJ, Simpson AJ, Marie SK: Cancer-testis (CT) antigen expression in medulloblastoma. Cancer Immun; 2008;8:7
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  • [Title] Cancer-testis (CT) antigen expression in medulloblastoma.
  • Medulloblastoma is the most common childhood malignant tumor of the central nervous system.
  • Treatment of medulloblastoma requires harmful therapy and nevertheless carries a poor prognosis.
  • Due to their presence in various cancers and their limited expression in normal tissues, CT antigens are ideal vaccine targets for tumor immunotherapy.
  • CT antigens, such as MAGE and NY-ESO-1, have been employed in clinical trials in various malignancies but little is known about their presence in medulloblastoma.
  • We analyzed 25 medulloblastomas for the expression of a panel of CT antigens by RT-PCR and immunohistochemistry.
  • The absence of correlation between mRNA and protein expression in medulloblastoma has not been observed in other tumors and further studies addressing the biology of CT antigens are necessary to investigate the present discrepant results.
  • [MeSH-major] Antigens, Neoplasm / biosynthesis. Cerebellar Neoplasms / immunology. Medulloblastoma / immunology
  • [MeSH-minor] Adult. Cancer Vaccines. Child. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Membrane Proteins / biosynthesis. Membrane Proteins / genetics. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. RNA Processing, Post-Transcriptional / genetics. RNA, Messenger / metabolism. Testis / metabolism. Testis / pathology

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  • (PMID = 18426187.001).
  • [ISSN] 1424-9634
  • [Journal-full-title] Cancer immunity
  • [ISO-abbreviation] Cancer Immun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / CTAG1B protein, human; 0 / Cancer Vaccines; 0 / MAGEA3 protein, human; 0 / MAGEC1 protein, human; 0 / MAGEC2 protein, human; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC2935780
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41. Baryawno N, Sveinbjörnsson B, Eksborg S, Orrego A, Segerström L, Oqvist CO, Holm S, Gustavsson B, Kågedal B, Kogner P, Johnsen JI: Tumor-growth-promoting cyclooxygenase-2 prostaglandin E2 pathway provides medulloblastoma therapeutic targets. Neuro Oncol; 2008 Oct;10(5):661-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor-growth-promoting cyclooxygenase-2 prostaglandin E2 pathway provides medulloblastoma therapeutic targets.
  • Prostaglandin E(2) (PGE(2)) has been shown to play important roles in several aspects of tumor development and progression.
  • In this study, we show for the first time that medulloblastoma (MB), the most common malignant childhood brain tumor, expresses high levels of COX-2, microsomal prostaglandin E synthase-1, and EP(1) through EP(4) and secretes PGE(2).
  • EP(1) and EP(3) receptor antagonists ONO-8713 and ONO-AE3-240, but not the EP(4) antagonists ONO-AE3-208 and AH 23848, inhibited tumor cell proliferation, indicating the significance of EP(1) and EP(3) but not EP(4) for MB growth.
  • [MeSH-major] Cerebellar Neoplasms / metabolism. Cyclooxygenase 2 / metabolism. Dinoprostone / metabolism. Medulloblastoma / metabolism. Signal Transduction / physiology
  • [MeSH-minor] Adolescent. Adult. Animals. Apoptosis / drug effects. Apoptosis / physiology. Blotting, Western. Cell Proliferation / drug effects. Child. Child, Preschool. Enzyme Inhibitors / pharmacology. Female. Flow Cytometry. Humans. Immunohistochemistry. Infant. Infant, Newborn. Male. Mice. Mice, Nude. Middle Aged. Xenograft Model Antitumor Assays

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  • (PMID = 18715952.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; EC 1.14.99.1 / Cyclooxygenase 2; K7Q1JQR04M / Dinoprostone
  • [Other-IDs] NLM/ PMC2666243
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42. Riazmontazer N, Daneshbod Y: Cytology of desmoplastic medulloblastoma in imprint smears: a report of 2 cases. Acta Cytol; 2006 Jan-Feb;50(1):97-100
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytology of desmoplastic medulloblastoma in imprint smears: a report of 2 cases.
  • BACKGROUND: Desmoplastic medulloblastoma is a rare subtype of medulloblastoma with astroglial differentiation.
  • The cytomorphologic features in intraoperative imprint smears from 2 cases of desmoplastic medulloblastoma are described.
  • CASE REPORTS: A 22-year-old man and 27-year-old woman with a cerebellar tumor underwent craniotomy and tumor resection.
  • The cytology was misinterpreted as glial tumors, while the final histologic diagnosis in both cases were desmoplastic medulloblastoma.
  • CONCLUSION: Desmoplastic medulloblastoma shows distinctive cytology in intraoperative smears.
  • However, the occurrence of this rare type in adults and the presence of astroglial elements in imprint smears may cause a cytologic misinterpretation as gliomas.
  • [MeSH-major] Cerebellar Neoplasms / diagnosis. Medulloblastoma / diagnosis
  • [MeSH-minor] Adult. Astrocytes / pathology. Brain Neoplasms / diagnosis. Diagnostic Errors. Female. Glioma / diagnosis. Humans. Intraoperative Period. Male. Neurons / pathology

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  • (PMID = 16514849.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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43. Gururangan S, Krauser J, Watral MA, Driscoll T, Larrier N, Reardon DA, Rich JN, Quinn JA, Vredenburgh JJ, Desjardins A, McLendon RE, Fuchs H, Kurtzberg J, Friedman HS: Efficacy of high-dose chemotherapy or standard salvage therapy in patients with recurrent medulloblastoma. Neuro Oncol; 2008 Oct;10(5):745-51
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  • [Title] Efficacy of high-dose chemotherapy or standard salvage therapy in patients with recurrent medulloblastoma.
  • The efficacy of high-dose chemotherapy (HDC) or standard salvage therapy was evaluated in patients with recurrent medulloblastoma (MBL) using retrospective chart review of all patients with recurrent MBL treated at Duke University Medical Center between 1995 and 2005 and who had undergone HDC with or without radiotherapy (RT) or standard salvage therapy after relapse.
  • All patients in groups B and C have died of tumor, at a median of 35 months and 26 months from HDC and standard salvage therapy, respectively.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Cerebellar Neoplasms / drug therapy. Medulloblastoma / drug therapy. Neoplasm Recurrence, Local / drug therapy. Salvage Therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Combined Modality Therapy. Disease-Free Survival. Humans. Kaplan-Meier Estimate. Retrospective Studies

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  • (PMID = 18755919.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2666251
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44. Kool M, Koster J, Bunt J, Hasselt NE, Lakeman A, van Sluis P, Troost D, Meeteren NS, Caron HN, Cloos J, Mrsić A, Ylstra B, Grajkowska W, Hartmann W, Pietsch T, Ellison D, Clifford SC, Versteeg R: Integrated genomics identifies five medulloblastoma subtypes with distinct genetic profiles, pathway signatures and clinicopathological features. PLoS One; 2008;3(8):e3088
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Integrated genomics identifies five medulloblastoma subtypes with distinct genetic profiles, pathway signatures and clinicopathological features.
  • BACKGROUND: Medulloblastoma is the most common malignant brain tumor in children.
  • This illustrates the potential benefits of a robust classification of medulloblastoma patients and a detailed knowledge of associated biological mechanisms.
  • METHODS AND FINDINGS: To get a better insight into the molecular biology of medulloblastoma we established mRNA expression profiles of 62 medulloblastomas and analyzed 52 of them also by comparative genomic hybridization (CGH) arrays.
  • Mutations in beta-catenin were identified in all 9 type A tumors, but not in any other tumor.
  • Monosomy of chromosome 6 occurred only in type A tumors, loss of 9q mostly occurred in type B tumors, whereas chromosome 17 aberrations, most common in medulloblastoma, were strongly associated with type C or D tumors.
  • We validated and confirmed the molecular subtypes and their associated clinicopathological features with expression data from a second independent series of 46 medulloblastomas.
  • CONCLUSIONS: The new medulloblastoma classification presented in this study will greatly enhance the understanding of this heterogeneous disease.
  • [MeSH-major] Cerebellar Neoplasms / genetics. Gene Expression Profiling. Genomics. Medulloblastoma / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. DNA Mutational Analysis. DNA, Neoplasm / genetics. Female. Humans. Male. Nucleic Acid Hybridization. RNA, Neoplasm / genetics. Signal Transduction. Transforming Growth Factor beta / physiology

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  • (PMID = 18769486.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / RNA, Neoplasm; 0 / Transforming Growth Factor beta
  • [Other-IDs] NLM/ PMC2518524
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45. Nakahara Y, Northcott PA, Li M, Kongkham PN, Smith C, Yan H, Croul S, Ra YS, Eberhart C, Huang A, Bigner D, Grajkowska W, Van Meter T, Rutka JT, Taylor MD: Genetic and epigenetic inactivation of Kruppel-like factor 4 in medulloblastoma. Neoplasia; 2010 Jan;12(1):20-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic and epigenetic inactivation of Kruppel-like factor 4 in medulloblastoma.
  • Although medulloblastoma is the most common pediatric malignant brain tumor, its molecular underpinnings are largely unknown.
  • We have identified rare, recurrent homozygous deletions of Kruppel-like Factor 4 (KLF4) in medulloblastoma using high-resolution single nucleotide polymorphism arrays, digital karyotyping, and genomic real-time polymerase chain reaction (PCR).
  • Furthermore, we show that there is loss of physiological KLF4 expression in more than 40% of primary medulloblastomas both at the RNA and protein levels.
  • Medulloblastoma cell lines drastically increase the expression of KLF4 in response to the demethylating agent 5-azacytidine and demonstrate dense methylation of the promoter CpG island by bisulfite sequencing.
  • Methylation-specific PCR targeting the KLF4 promoter demonstrates CpG methylation in approximately 16% of primary medulloblastomas.
  • Reexpression of KLF4 in the D283 medulloblastoma cell line results in significant growth suppression both in vitro and in vivo.
  • We conclude that KLF4 is inactivated by either genetic or epigenetic mechanisms in a large subset of medulloblastomas and that it likely functions as a tumor suppressor gene in the pathogenesis of medulloblastoma.
  • [MeSH-major] Cerebellar Neoplasms / genetics. Epigenesis, Genetic. Kruppel-Like Transcription Factors / genetics. Medulloblastoma / genetics
  • [MeSH-minor] Adult. Animals. Antimetabolites, Antineoplastic / pharmacology. Azacitidine / pharmacology. Cell Line, Tumor. CpG Islands / genetics. DNA Methylation / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic / genetics. Humans. Kaplan-Meier Estimate. Loss of Heterozygosity. Mice. Mice, Nude. Neoplasms, Experimental / genetics. Neoplasms, Experimental / pathology. Oligonucleotide Array Sequence Analysis. Polymorphism, Single Nucleotide. Promoter Regions, Genetic / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transplantation, Heterologous

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  • (PMID = 20072650.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS055089
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / GKLF protein; 0 / Kruppel-Like Transcription Factors; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ PMC2805880
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46. Hamasaki K, Nakamura H, Ueda Y, Makino K, Kuratsu J: Radiation-induced glioblastoma occurring 35 years after radiation therapy for medulloblastoma: case report. Brain Tumor Pathol; 2010 Apr;27(1):39-43
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  • [Title] Radiation-induced glioblastoma occurring 35 years after radiation therapy for medulloblastoma: case report.
  • Histological diagnosis was medulloblastoma (MB).
  • Postoperatively he received a total of 40 Gy radiation to the whole brain and 30.5 Gy to the spine without chemotherapy.
  • The tumor was surgically removed, and he received radiotherapy and chemotherapy with ACNU, procarbazine, and vincristine.
  • Postoperative irradiation reduced the size of the second tumor.
  • [MeSH-major] Cerebellar Neoplasms / therapy. Glioblastoma / etiology. Glioblastoma / therapy. Medulloblastoma / radiotherapy. Neoplasms, Second Primary. Radiotherapy / adverse effects
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Male. Neurosurgical Procedures. Nimustine / administration & dosage. Procarbazine / administration & dosage. Time Factors. Treatment Outcome. Vincristine / administration & dosage

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  • (PMID = 20425047.001).
  • [ISSN] 1861-387X
  • [Journal-full-title] Brain tumor pathology
  • [ISO-abbreviation] Brain Tumor Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0S726V972K / Nimustine; 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine
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47. Ang C, Hauerstock D, Guiot MC, Kasymjanova G, Roberge D, Kavan P, Muanza T: Characteristics and outcomes of medulloblastoma in adults. Pediatr Blood Cancer; 2008 Nov;51(5):603-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characteristics and outcomes of medulloblastoma in adults.
  • BACKGROUND: Adult medulloblastoma is a rare disease for which there is no internationally accepted standard of care.
  • We sought to review the presentation, management, and outcome of patients with adult medulloblastoma treated at the McGill University teaching hospitals over the past 18 years.
  • METHODS: Medical records were reviewed to gather demographic and clinical data including presenting symptoms, tumor characteristics, management, survival, and treatment toxicity.
  • CONCLUSION: Adult medulloblastoma has distinct characteristics from the pediatric population including presentation in the lateral cerebellar hemispheres.
  • [MeSH-major] Cerebellar Neoplasms / pathology. Cerebellar Neoplasms / therapy. Medulloblastoma / pathology. Medulloblastoma / therapy
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chemotherapy, Adjuvant / adverse effects. Combined Modality Therapy. Cranial Irradiation. Disease-Free Survival. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / pathology. Neoplasm Recurrence, Local / therapy. Neurosurgical Procedures. Radiotherapy, Adjuvant / adverse effects. Salvage Therapy / methods. Treatment Outcome

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18649371.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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48. Eberhart CG, Chaudhry A, Daniel RW, Khaki L, Shah KV, Gravitt PE: Increased p53 immunopositivity in anaplastic medulloblastoma and supratentorial PNET is not caused by JC virus. BMC Cancer; 2005 Feb 17;5:19
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased p53 immunopositivity in anaplastic medulloblastoma and supratentorial PNET is not caused by JC virus.
  • BACKGROUND: p53 mutations are relatively uncommon in medulloblastoma, but abnormalities in this cell cycle pathway have been associated with anaplasia and worse clinical outcomes.
  • We correlated p53 protein expression with pathological subtype and clinical outcome in 75 embryonal brain tumors.
  • METHODS: p53 protein levels were evaluated semi-quantitatively in 64 medulloblastomas, 3 atypical teratoid rhabdoid tumors (ATRT), and 8 supratentorial primitive neuroectodermal tumors (sPNET) using immunohistochemistry.
  • JC viral sequences were analyzed in DNA extracted from 33 frozen medulloblastoma and PNET samples using quantitative polymerase chain reaction.
  • RESULTS: p53 expression was detected in 18% of non-anaplastic medulloblastomas, 45% of anaplastic medulloblastomas, 67% of ATRT, and 88% of sPNET.
  • The increased p53 immunoreactivity in anaplastic medulloblastoma, ATRT, and sPNET was statistically significant.
  • No JC virus was identified in the embryonal brain tumor samples, while an endogenous human retrovirus (ERV-3) was readily detected.
  • CONCLUSION: Immunoreactivity for p53 protein is more common in anaplastic medulloblastomas, ATRT and sPNET than in non-anaplastic tumors, and is associated with worse clinical outcomes.

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  • (PMID = 15717928.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / K08 NS043279; United States / NINDS NIH HHS / NS / K08NS43279
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC554768
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49. Khalil EM: Treatment results of adults and children with medulloblastoma NCI, Cairo University experience. J Egypt Natl Canc Inst; 2008 Jun;20(2):175-86
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  • [Title] Treatment results of adults and children with medulloblastoma NCI, Cairo University experience.
  • PURPOSE: To evaluate treatment outcome and prognostic factors of adults and pediatric medulloblastoma patients treated by adjuvant postoperative craniospinal irradiation (CSI) and chemotherapy.
  • PATIENTS AND METHODS: Between 1997 and 2004, 67 patients were treated in the National cancer Institute- Cairo University; 51 pediatric patients with a median age of 7 years and 16 adult patients with a median age of 25 years.
  • According to the Chang staging system; 50%-35% , 37.5%-47% and 12.5%-18% had T2, T3 and T4 tumors of adults and pediatric patient's population respectively.
  • All patients underwent primary surgical resection; near total resection in 25% , Subtotal resection in 61% ; with tumor residual < 1.5cm(2) in 49% compared to 51% with > 1.5cm(2) residual tumor and 14% , had biopsy only.
  • All patients were treated by craniospinal radiotherapy (RT); with a median dose of 34Gy to the whole brain, 54Gy to the posterior fossa and 32Gy to the spinal axis.
  • The median interval between surgery and RT was 45 days and 38 days for the pediatric and adult groups respectively.
  • The median duration of RT was 54 days and 52 days for pediatric and adult patients respectively.
  • RESULTS: For the pediatric and adult patients, the 5- and 7-year overall and disease-free survival rates were 89% & 78% vs. 84% & 56% and 80% & 68% vs. 79% & 52% respectively.
  • Fourteen patients (21% ) relapsed (10 pediatric and 4 adults) at a median time of 11 months vs. 23 months and a median follow-up period of 8 and 12 months respectively; Neuro-axis was the most common site of relapse (11 patients).
  • Ninety percent (9/10) of the pediatric relapses were of the high risk group (8 received no chemotherapy) and took place within 2 years; similarly all adult relapses were of the high risk group; three relapses took place after 2 years.
  • For adult patients; only the risk category was a significant prognostic factor with 5-year disease-free survival rate of 100% vs. 40% for low and high risk respectively (p=0.03).
  • CONCLUSION: Survival rates of medulloblastoma pediatric patients were better than the adult ones.
  • Late relapses, lateral tumor location and shorter median follow up were noted in adult patients.
  • Advanced tumor stage, metastases at presentation, limited tumor resection were powerful prognostic factors among the pediatric patients.
  • In addition, high risk category was shown to be a prognostic factor for both pediatric and adult patients.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cerebellar Neoplasms / therapy. Cranial Irradiation. Medulloblastoma / therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Combined Modality Therapy. Female. Follow-Up Studies. Humans. Male. Neoplasm Recurrence, Local / diagnosis. Neoplasm Recurrence, Local / therapy. Neoplasm Staging. Prognosis. Radiotherapy Dosage. Radiotherapy, Adjuvant. Survival Rate. Treatment Outcome. Young Adult

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  • (PMID = 20029474.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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50. Rodriguez FJ, Eberhart C, O'Neill BP, Slezak J, Burger PC, Goldthwaite P, Wu W, Giannini C: Histopathologic grading of adult medulloblastomas. Cancer; 2007 Jun 15;109(12):2557-65
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  • [Title] Histopathologic grading of adult medulloblastomas.
  • BACKGROUND: Histopathologic evaluation of the degree and extent of anaplasia is a useful prognostic parameter in pediatric medulloblastomas.
  • Whether the same applies to adult medulloblastomas is not known.
  • METHODS: The study included 74 adult patients with histologically confirmed medulloblastomas and retrospectively reassessed 67 cases with available slides for the presence of nodularity, collagen deposition (desmoplasia without nodules), and degree and extent of anaplasia.
  • CONCLUSIONS: The incidence of severe anaplasia in adult medulloblastomas is lower than in the pediatric population.
  • [MeSH-major] Cerebellar Neoplasms / classification. Medulloblastoma / classification
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Aged. Female. Humans. Immunoenzyme Techniques. Incidence. Male. Middle Aged. Neoplasm Staging. Prognosis. Retrospective Studies. Sex Distribution. Survival Rate

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  • [Copyright] Copyright 2007 American Cancer Society.
  • (PMID = 17487854.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
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51. Lindsey JC, Lusher ME, Anderton JA, Gilbertson RJ, Ellison DW, Clifford SC: Epigenetic deregulation of multiple S100 gene family members by differential hypomethylation and hypermethylation events in medulloblastoma. Br J Cancer; 2007 Jul 16;97(2):267-74
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  • [Title] Epigenetic deregulation of multiple S100 gene family members by differential hypomethylation and hypermethylation events in medulloblastoma.
  • Using a pharmacological expression reactivation approach, we screened 16 S100 genes for evidence of epigenetic regulation in medulloblastoma, the most common malignant brain tumour of childhood.
  • Four family members (S100A2, S100A4, S100A6 and S100A10) demonstrated evidence of upregulated expression in multiple medulloblastoma cell lines, following treatment with the DNA methyltransferase inhibitor, 5'-aza-2'-deoxycytidine.
  • Assessment of these genes in the non-neoplastic cerebellum (from which medulloblastomas develop) revealed strong somatic methylation affecting S100A2 and S100A4, whereas S100A6 and S100A10 were unmethylated.
  • Assessed against these normal tissue-specific methylation states, S100A6 and S100A10 demonstrated tumour-specific hypermethylation in medulloblastoma primary tumours (5 out of 40 and 4 out of 35, respectively, both 12%) and cell lines (both 7 out of 9, 78%), which was associated with their transcriptional silencing.
  • In summary, these data characterise complex patterns of somatic methylation affecting S100 genes in the normal cerebellum and demonstrate their disruption causing epigenetic deregulation of multiple S100 family members in medulloblastoma development.
  • [MeSH-major] Cerebellar Neoplasms / genetics. Epigenesis, Genetic. Gene Expression Regulation, Neoplastic. Medulloblastoma / genetics. S100 Proteins / genetics
  • [MeSH-minor] Adolescent. Adult. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Cell Line, Tumor. Cerebellum / metabolism. Child. Child, Preschool. DNA Methylation. DNA Modification Methylases / antagonists & inhibitors. Female. Humans. Infant. Male

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  • (PMID = 17579622.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / S100 Proteins; 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ PMC2360310
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52. Maddrey AM, Bergeron JA, Lombardo ER, McDonald NK, Mulne AF, Barenberg PD, Bowers DC: Neuropsychological performance and quality of life of 10 year survivors of childhood medulloblastoma. J Neurooncol; 2005 May;72(3):245-53
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  • [Title] Neuropsychological performance and quality of life of 10 year survivors of childhood medulloblastoma.
  • PURPOSE: Survivors of medulloblastoma, the most frequently occurring malignant brain tumor of childhood, suffer neuropsychological damage in the first decade after diagnosis.
  • Cognitive performance, psychosocial functioning and quality of life were assessed in medulloblastoma survivors in the second decade after diagnosis.
  • RESULTS: Sixteen medulloblastoma survivors [mean age at diagnosis: 7.2 years, range: 1-15 years; 6 males] were tested at a mean age of 22.2 years [range: 13.6-27.9 years].
  • CONCLUSION: Survivors of childhood medulloblastoma frequently suffer severe persistent deficits in a wide-range of neuropsychological functional domains.
  • These severe neuropsychological and psychosocial deficiencies justify further attempts to reduce or delay the use of craniospinal radiation therapy for childhood medulloblastoma.
  • [MeSH-major] Cerebellar Neoplasms / psychology. Medulloblastoma / psychology. Quality of Life. Survivors / psychology
  • [MeSH-minor] Activities of Daily Living. Adult. Child. Cognition / physiology. Cognition Disorders / etiology. Cognition Disorders / psychology. Education. Employment. Female. Humans. Intelligence Tests. Interpersonal Relations. Male. Neuropsychological Tests. Psychomotor Performance / physiology. Surveys and Questionnaires

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  • (PMID = 15937648.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
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53. Matsumoto J, Kochi M, Morioka M, Nakamura H, Makino K, Hamada J, Kuratsu J, Ushio Y: A long-term ventricular drainage for patients with germ cell tumors or medulloblastoma. Surg Neurol; 2006 Jan;65(1):74-80; discussion 80
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  • [Title] A long-term ventricular drainage for patients with germ cell tumors or medulloblastoma.
  • BACKGROUND: Hydrocephalus associated with intracranial germ cell tumors or disseminated medulloblastoma has been treated with ventriculoperitoneal shunt.
  • However, this procedure has a potential risk of intraperitoneal metastasis of these brain tumors.
  • METHODS: From 1979 to 2003, we have treated 96 patients with germ cell tumors and medulloblastoma in our hospital.
  • Of 96 patients, 59 (germ cell tumor, 31; medulloblastoma, 28) had hydrocephalus and 13 needed long-term cerebrospinal fluid drainage to manage the obstructive hydrocephalus due to persistent tumor or communicating hydrocephalus due to dissemination.
  • We performed PLTVD for these cases using a flow-controlled shunt device and percutaneous long-tunneled shunt tube (peritoneal catheter) exiting at the upper abdomen and connecting to a closed drainage system.
  • CONCLUSIONS: Percutaneous long-tunneled ventricular drainage was an effective method to manage long-lasting obstructive or communicating hydrocephalus with germ cell tumors and medulloblastoma.
  • [MeSH-major] Brain Neoplasms / complications. Hydrocephalus / etiology. Hydrocephalus / surgery. Medulloblastoma / complications. Neoplasms, Germ Cell and Embryonal / complications. Ventriculoperitoneal Shunt
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Humans. Incidence. Infant. Infection / epidemiology. Male. Postoperative Complications / epidemiology. Retrospective Studies. Time Factors


54. Jouanneau E, Guzman Tovar RA, Desuzinges C, Frappaz D, Louis-Tisserand G, Sunyach MP, Jouvet A, Sindou M: Very late frontal relapse of medulloblastoma mimicking a meningioma in an adult: usefulness of 1H magnetic resonance spectroscopy and diffusion-perfusion magnetic resonance imaging for preoperative diagnosis: case report. Neurosurgery; 2006 Apr;58(4):E789; discussion E789
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  • [Title] Very late frontal relapse of medulloblastoma mimicking a meningioma in an adult: usefulness of 1H magnetic resonance spectroscopy and diffusion-perfusion magnetic resonance imaging for preoperative diagnosis: case report.
  • OBJECTIVE AND IMPORTANCE: We present a rare case of very long-term medulloblastoma relapse in an adult patient and discuss the pattern of recurrence and metabolic imaging of the tumor.
  • CLINICAL PRESENTATION: A 45-year-old man was referred for evaluation of a frontobasal midline tumor 21 years after treatment of a cerebellar medulloblastoma by surgery followed by chemotherapy and craniospinal radiotherapy.
  • Several hypotheses were discussed, such as other radio-induced tumors, sarcomas, high-grade gliomas, or lymphomas (previous chemotherapy) and even recurrence of medulloblastoma.
  • On diffusion imaging, the tumor appeared hyperintense, with a low apparent diffusion coefficient value of 0.689.
  • Metabolic imaging favored the diagnosis of medulloblastoma over the initially suspected diagnosis of meningioma.
  • The patient underwent complete removal of the tumor that was confirmed to be a metastasis of his primary medulloblastoma.
  • CONCLUSION: Late relapse should be considered, even after several decades, on occurrence of a second intracranial tumor in this context.
  • Our observation validates the clinical interest of preoperative metabolic imaging for brain tumors with distinctive pattern.
  • [MeSH-major] Cerebellar Neoplasms / diagnosis. Medulloblastoma / diagnosis. Meningeal Neoplasms / diagnosis. Meningioma / diagnosis

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  • (PMID = 16575298.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protons
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55. Rieken S, Gaiser T, Mohr A, Welzel T, Witt O, Kulozik AE, Wick W, Debus J, Combs SE: Outcome and prognostic factors of desmoplastic medulloblastoma treated within a multidisciplinary treatment concept. BMC Cancer; 2010;10:450
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  • [Title] Outcome and prognostic factors of desmoplastic medulloblastoma treated within a multidisciplinary treatment concept.
  • BACKGROUND: Desmoplasia in medulloblastoma is often diagnosed in adult patients and was repeatedly associated with improved results.
  • Today, all medulloblastoma patients receive intensive multimodal treatment including surgery, radiotherapy and chemotherapy.
  • This study was set up to investigate treatment outcome and prognostic factors after radiation therapy in patients with desmoplastic medulloblastomas.
  • METHODS: Twenty patients treated for desmoplastic medulloblastoma in the Department of Radiation Oncology at the University of Heidelberg between 1984 and 2007 were included.
  • Tumor resection was performed in all patients.
  • Two patients underwent whole brain radiotherapy (WBRT), and 18 patients received craniospinal irradiation (CSI).
  • The median dose to the whole brain and the craniospinal axis was 35.2 Gray (Gy), and 54.4 Gy to the posterior fossa.
  • Five patients died from recurrent medulloblastoma.
  • CONCLUSIONS: Multimodal approaches with surgical resection followed by chemoirradiation achieved high response rates with long OS in desmoplastic medulloblastoma patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cerebellar Neoplasms / therapy. Cranial Irradiation. Medulloblastoma / therapy. Neoplasm Recurrence, Local / therapy. Neurosurgical Procedures
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Combined Modality Therapy. Female. Humans. Male. Middle Aged. Neoplasm Staging. Radiotherapy Dosage. Retrospective Studies. Survival Rate. Treatment Outcome. Young Adult

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  • (PMID = 20731859.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2939548
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56. De Bortoli M, Castellino RC, Lu XY, Deyo J, Sturla LM, Adesina AM, Perlaky L, Pomeroy SL, Lau CC, Man TK, Rao PH, Kim JY: Medulloblastoma outcome is adversely associated with overexpression of EEF1D, RPL30, and RPS20 on the long arm of chromosome 8. BMC Cancer; 2006 Sep 12;6:223
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  • [Title] Medulloblastoma outcome is adversely associated with overexpression of EEF1D, RPL30, and RPS20 on the long arm of chromosome 8.
  • BACKGROUND: Medulloblastoma is the most common malignant brain tumor of childhood.
  • In the present study, we applied cytogenetic characterization to guide the identification of biologically significant genes from gene expression microarray profiles of medulloblastoma.
  • METHODS: We analyzed 71 primary medulloblastomas for chromosomal copy number aberrations (CNAs) using comparative genomic hybridization (CGH).
  • By applying CGH results to gene expression analysis of medulloblastoma, we identified three 8q-mapped genes that are associated with overall survival in the larger group of 64 patients (p < 0.05): eukaryotic translation elongation factor 1D (EEF1D), ribosomal protein L30 (RPL30), and ribosomal protein S20 (RPS20).
  • CONCLUSION: The complementary use of CGH and expression profiles can facilitate the identification of clinically significant candidate genes involved in medulloblastoma growth.
  • We demonstrate that gain of 8q and expression levels of three 8q-mapped candidate genes (EEF1D, RPL30, RPS20) are associated with adverse outcome in medulloblastoma.

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  • (PMID = 16968546.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA105607; United States / NICHD NIH HHS / HD / HD042977; United States / NINDS NIH HHS / NS / NS043517; United States / NICHD NIH HHS / HD / T32 HD042977; United States / NCI NIH HHS / CA / R01 CA105607; United States / NINDS NIH HHS / NS / K08 NS043517; United States / NICHD NIH HHS / HD / K12 HD041648; United States / NCI NIH HHS / CA / R01 CA109467; United States / NICHD NIH HHS / HD / HD041648; United States / NCI NIH HHS / CA / CA109467
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Peptide Elongation Factor 1; 0 / Ribosomal Proteins; 0 / ribosomal protein L30; 0 / ribosomal protein S20
  • [Other-IDs] NLM/ PMC1578584
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57. Bobola MS, Finn LS, Ellenbogen RG, Geyer JR, Berger MS, Braga JM, Meade EH, Gross ME, Silber JR: Apurinic/apyrimidinic endonuclease activity is associated with response to radiation and chemotherapy in medulloblastoma and primitive neuroectodermal tumors. Clin Cancer Res; 2005 Oct 15;11(20):7405-14
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  • [Title] Apurinic/apyrimidinic endonuclease activity is associated with response to radiation and chemotherapy in medulloblastoma and primitive neuroectodermal tumors.
  • We assayed apurinic/apyrimidinic endonuclease activity in medulloblastomas and primitive neuroectodermal tumors (PNET) to establish correlates with tumor and patient characteristics and with response to adjuvant radiation plus multiagent chemotherapy.
  • EXPERIMENTAL DESIGN: Ap endo activity was assayed in 52 medulloblastomas and 10 PNETs from patients 0.4 to 21 years old.
  • Ape1/Ref-1, the predominant human Ap endo activity, was measured in 42 medulloblastomas by immunostaining.
  • Cox proportional hazards regression models were used to analyze the association of activity with time to tumor progression (TTP).
  • RESULTS: Tumor Ap endo activity varied 180-fold and was significantly associated with age and gender.
  • Tumor Ape1/Ref-1 was detected almost exclusively in nuclei.
  • In a multivariate model, with Ap endo activity entered as a continuous variable, the hazard ratio for progression after adjuvant treatment in 46 medulloblastomas and four PNETs increased by a factor of 1.073 for every 0.01 unit increase in activity (P < or = 0.001) and was independent of age and gender.
  • Suppressing Ap endo activity in a human medulloblastoma cell line significantly increased sensitivity to 1,3-bis(2-chlororethyl)-1-nitrosourea and temozolomide, suggesting that the association of tumor activity with TTP reflected, at least in part, abasic site repair.
  • CONCLUSIONS: Our data (a) suggest that Ap endo activity promotes resistance to radiation plus chemotherapy in medulloblastomas/PNETs, (b) provide a potential marker of treatment outcome, and (c) suggest clinical use of Ap endo inhibitors to overcome resistance.
  • [MeSH-major] Brain Neoplasms / enzymology. DNA-(Apurinic or Apyrimidinic Site) Lyase / metabolism. Medulloblastoma / enzymology. Neuroectodermal Tumors, Primitive / enzymology
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents, Alkylating / pharmacology. Blotting, Western. Brain / drug effects. Brain / enzymology. Brain / radiation effects. Carmustine / pharmacology. Cell Line, Tumor. Cell Nucleus / enzymology. Cell Survival / drug effects. Cell Survival / genetics. Child. Child, Preschool. Combined Modality Therapy. Disease Progression. Dose-Response Relationship, Drug. Female. Humans. Immunohistochemistry. Infant. Infant, Newborn. Male. Multivariate Analysis. Oligonucleotides, Antisense / genetics. RNA, Small Interfering / genetics. Time Factors. Transfection

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  • (PMID = 16243814.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA104593; United States / NCI NIH HHS / CA / CA70790; United States / NCI NIH HHS / CA / CA82622
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Oligonucleotides, Antisense; 0 / RNA, Small Interfering; EC 4.2.99.18 / DNA-(Apurinic or Apyrimidinic Site) Lyase; U68WG3173Y / Carmustine
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58. Hartmann W, Digon-Söntgerath B, Koch A, Waha A, Endl E, Dani I, Denkhaus D, Goodyer CG, Sörensen N, Wiestler OD, Pietsch T: Phosphatidylinositol 3'-kinase/AKT signaling is activated in medulloblastoma cell proliferation and is associated with reduced expression of PTEN. Clin Cancer Res; 2006 May 15;12(10):3019-27
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  • [Title] Phosphatidylinositol 3'-kinase/AKT signaling is activated in medulloblastoma cell proliferation and is associated with reduced expression of PTEN.
  • PURPOSE: Medulloblastomas represent the most frequent malignant brain tumors of childhood.
  • Recently, it has been shown that Sonic Hedgehog-induced formation of medulloblastoma in an animal model is significantly enhanced by activation of the phosphatidylinositol 3'-kinase (PI3K) signaling pathway.
  • EXPERIMENTAL DESIGN: To examine a role for PI3K/AKT signaling in the molecular pathogenesis of human medulloblastoma, we did an immunohistochemical study of the expression of Ser473-phosphorylated (p)-AKT protein in 22 medulloblastoma samples: All samples displayed p-AKT expression.
  • To investigate if an activated PI3K/AKT pathway is required for medulloblastoma cell growth, we treated five human medulloblastoma cell lines with increasing concentrations of the PI3K inhibitor LY294002 and analyzed cellular proliferation and apoptosis.
  • As the activation of PI3K/AKT signaling may be associated with alterations of the PTEN gene located at 10q23.3, a chromosomal region subject to frequent allelic losses in medulloblastoma, we screened PTEN for mutations and mRNA expression.
  • RESULTS: Proliferation of all of the medulloblastoma cell lines was dependent on PI3K/AKT signaling, whereas apoptosis was not prominently affected.
  • One medulloblastoma cell line was found to carry a truncating mutation in the PTEN coding sequence.
  • Even more important, PTEN mRNA and protein levels were found to be significantly lower in medulloblastomas compared with normal cerebellar tissue of different developmental stages.
  • Reduction of PTEN expression was found to be associated with PTEN promoter hypermethylation in 50% of the tumor samples.
  • CONCLUSIONS: We conclude that activation of the PI3K/AKT pathway constitutes an important step in the molecular pathogenesis of medulloblastoma and that dysregulation of PTEN may play a significant role in this context.
  • [MeSH-major] Cell Proliferation. Cerebellar Neoplasms / metabolism. Medulloblastoma / metabolism. PTEN Phosphohydrolase / genetics. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism
  • [MeSH-minor] Adult. Child. DNA Mutational Analysis. Humans. Immunohistochemistry. Loss of Heterozygosity. Polymerase Chain Reaction. Polymorphism, Genetic. Signal Transduction. Tumor Cells, Cultured

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  • (PMID = 16707597.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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59. Selek U, Zorlu F, Hurmuz P, Cengiz M, Turker A, Soylemezoglu F, Gurkaynak M: Craniospinal radiotherapy in adult medulloblastoma. Strahlenther Onkol; 2007 May;183(5):236-40
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  • [Title] Craniospinal radiotherapy in adult medulloblastoma.
  • PURPOSE: To evaluate the outcome and prognostic factors of adult patients with medulloblastoma.
  • PATIENTS AND METHODS: 26 adult medulloblastoma patients with a median age of 27 were subjected to craniospinal radiotherapy.
  • Patient characteristics, treatment factors and tumor characteristics failed to show any significance in univariate analysis.
  • [MeSH-major] Cerebellar Neoplasms / radiotherapy. Cranial Irradiation. Medulloblastoma / radiotherapy. Spine / radiation effects
  • [MeSH-minor] Adolescent. Adult. Cohort Studies. Combined Modality Therapy. Disease-Free Survival. Female. Humans. Male. Prognosis. Radiotherapy Dosage. Radiotherapy, Adjuvant. Retrospective Studies. Survival Rate. Treatment Outcome

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  • (PMID = 17497094.001).
  • [ISSN] 0179-7158
  • [Journal-full-title] Strahlentherapie und Onkologie : Organ der Deutschen Röntgengesellschaft ... [et al]
  • [ISO-abbreviation] Strahlenther Onkol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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60. Ongürü O, Karslioglu Y, Ozcan A, Celik E: Anti-apoptotic and growth-promoting markers in adult medulloblastomas. Clin Neuropathol; 2010 Nov-Dec;29(6):384-9
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  • [Title] Anti-apoptotic and growth-promoting markers in adult medulloblastomas.
  • AIM: the aim of this study was to investigate the pathologic features, proliferation potential and expression of some anti-apoptotic and growth-promoting markers in adult medulloblastomas.
  • METHOD: we analyzed the immunohistochemical expression of survivin, c-KIT, Bcl-2, fascin, p-53 and Ki-67 in 18 adult medulloblastomas (> 16 years of age).
  • 14 cases were classical, 2 desmoplastic/nodular and 2 large cell medulloblastomas.
  • Moderate-to-high nuclear survivin expression was observed with high percentages (55 - 100%) in all medulloblastomas while Bcl-2 was mildly positive in only 1 case.
  • Fascin expression was observed in 13 medulloblastomas (72%), 9 of which showing moderate to high immunoreactivity.
  • CONCLUSION: frequent nuclear survivin expression implies the predominance of anti-apoptotic factors in pathogenesis of adult medulloblastomas.
  • It may also be a potential therapeutic target for adult medulloblastomas.
  • Although Blc-2 immunoreactivity was previously reported in approximately 30% in medulloblastomas, we have observed that it is rarely expressed in the present series of adult medulloblastomas.
  • To our knowledge, this is the first study evaluating fascin expression in medulloblastomas.
  • Mild-to-moderate cytoplasmic c-KIT immunoreactivity without membranous staining in adult medulloblastomas may support the previous studies reporting low level of c-KIT protein expression with lack of activating mutations in medulloblastomas.
  • It seems p53 is rarely involved in the course of develepment of adult medulloblastomas.
  • [MeSH-major] Apoptosis Regulatory Proteins / metabolism. Cerebellar Neoplasms / metabolism. Growth Substances / metabolism. Medulloblastoma / metabolism
  • [MeSH-minor] Adolescent. Adult. Biomarkers, Tumor / metabolism. Carrier Proteins / metabolism. Female. Humans. Inhibitor of Apoptosis Proteins. Male. Microfilament Proteins / metabolism. Microtubule-Associated Proteins / metabolism. Middle Aged. Proto-Oncogene Proteins c-bcl-2 / metabolism. Proto-Oncogene Proteins c-kit / metabolism. Retrospective Studies. Tumor Suppressor Protein p53 / metabolism. Young Adult

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  • (PMID = 21073843.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Carrier Proteins; 0 / Growth Substances; 0 / Inhibitor of Apoptosis Proteins; 0 / Microfilament Proteins; 0 / Microtubule-Associated Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 146808-54-0 / fascin; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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61. Benesch M, Spiegl K, Winter A, Passini A, Lackner H, Moser A, Sovinz P, Schwinger W, Urban C: A scoring system to quantify late effects in children after treatment for medulloblastoma/ependymoma and its correlation with quality of life and neurocognitive functioning. Childs Nerv Syst; 2009 Feb;25(2):173-81
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  • [Title] A scoring system to quantify late effects in children after treatment for medulloblastoma/ependymoma and its correlation with quality of life and neurocognitive functioning.
  • BACKGROUND: The aim of this study was to quantify the severity of late effects by a simple numerical score (late effects severity score, LESS) in patients who received radiochemotherapy for medulloblastoma or ependymoma.
  • Twenty-three patients with medulloblastoma (n = 18) or ependymoma (n = 5) underwent extensive neurocognitive and QoL testing at a median of 56 months (range, 1-174) after the end of treatment.
  • Eight patients with low-grade glioma (LGG) who underwent tumor resection only served as control group.
  • RESULTS: Patients with medulloblastoma/ependymoma had significantly higher LESS and significantly lower Wechsler Adult Intelligence Scale (WAIS)/Wechsler Intelligence Scales for Children (WISC) scores compared to patients with LGG.
  • Comparison of QoL and late effects in patients with medulloblastoma/ependymoma demonstrated a significant negative correlation only for neurological late effects and the KINDL score suggesting that younger patients with more severe late effects reported on a worse QoL.
  • CONCLUSIONS: This LESS seems to be a simple and practical tool to quantify late effects in former brain tumor patients.
  • [MeSH-major] Ependymoma / therapy. Medulloblastoma / therapy. Nervous System Diseases / physiopathology. Quality of Life
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Cognition / drug effects. Cognition / physiology. Cognition / radiation effects. Combined Modality Therapy / adverse effects. Drug-Related Side Effects and Adverse Reactions. Endocrine System / drug effects. Endocrine System / physiopathology. Endocrine System / radiation effects. Female. Follow-Up Studies. Hearing / drug effects. Hearing / physiology. Hearing / radiation effects. Humans. Infant. Magnetic Resonance Imaging / methods. Male. Outcome Assessment (Health Care) / methods. Radiotherapy / adverse effects. Time Factors. Verbal Learning / drug effects. Verbal Learning / physiology. Verbal Learning / radiation effects. Vision, Ocular / drug effects. Vision, Ocular / physiology. Vision, Ocular / radiation effects. Young Adult

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  • (PMID = 18974990.001).
  • [ISSN] 1433-0350
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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62. Fouladi M, Nicholson HS, Zhou T, Laningham F, Helton KJ, Holmes E, Cohen K, Speights RA, Wright J, Pollack IF, Children's Oncology Group: A phase II study of the farnesyl transferase inhibitor, tipifarnib, in children with recurrent or progressive high-grade glioma, medulloblastoma/primitive neuroectodermal tumor, or brainstem glioma: a Children's Oncology Group study. Cancer; 2007 Dec 1;110(11):2535-41
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  • [Title] A phase II study of the farnesyl transferase inhibitor, tipifarnib, in children with recurrent or progressive high-grade glioma, medulloblastoma/primitive neuroectodermal tumor, or brainstem glioma: a Children's Oncology Group study.
  • BACKGROUND: An open-label Phase II study of tipifarnib was conducted to evaluate its safety and efficacy in children with recurrent or refractory medulloblastoma (MB)/primitive neuroectodermal tumor (PNET), high-grade glioma (HGG), and diffuse intrinsic brainstem glioma (BSG).
  • CONCLUSIONS: Tipifarnib tolerated well but had little activity as a single agent in children with recurrent central nervous system malignancies.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Brain Stem Neoplasms / drug therapy. Glioma / drug therapy. Medulloblastoma / drug therapy. Quinolones / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Disease Progression. Female. Humans. Male. Neuroectodermal Tumors / drug therapy. Treatment Outcome


63. Bunin GR, Kushi LH, Gallagher PR, Rorke-Adams LB, McBride ML, Cnaan A: Maternal diet during pregnancy and its association with medulloblastoma in children: a children's oncology group study (United States). Cancer Causes Control; 2005 Sep;16(7):877-91
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  • [Title] Maternal diet during pregnancy and its association with medulloblastoma in children: a children's oncology group study (United States).
  • Fruit, vegetables, vitamin C, and folate during pregnancy have been suggested as protective factors for medulloblastoma/primitive neuroectodermal tumor (PNET), a common brain tumor in children.
  • As hypothesized, cured meats were not associated with medulloblastoma/PNET, in contrast to other childhood brain tumors.
  • French fries (OR = 2.4, 95% CI: 1.2, 4.9) and chili peppers (OR = 1.8, 95% CI: 1.0, 3.0) were associated with medulloblastoma/PNET.
  • [MeSH-major] Cerebellar Neoplasms / epidemiology. Food Habits. Medulloblastoma / epidemiology
  • [MeSH-minor] Adult. Antioxidants / administration & dosage. Ascorbic Acid / administration & dosage. Candy / adverse effects. Female. Folic Acid / administration & dosage. Fruit. Humans. Maternal Welfare. Meat / adverse effects. Micronutrients. Odds Ratio. Pregnancy. United States / epidemiology. Vegetables. Vitamin B Complex / administration & dosage

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  • (PMID = 16132798.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA15488; United States / NCI NIH HHS / CA / CA60951
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Micronutrients; 12001-76-2 / Vitamin B Complex; 935E97BOY8 / Folic Acid; PQ6CK8PD0R / Ascorbic Acid
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64. Allen J, Donahue B, Mehta M, Miller DC, Rorke LB, Jakacki R, Robertson P, Sposto R, Holmes E, Vezina G, Muraszko K, Puccetti D, Prados M, Chan KW: A phase II study of preradiotherapy chemotherapy followed by hyperfractionated radiotherapy for newly diagnosed high-risk medulloblastoma/primitive neuroectodermal tumor: a report from the Children's Oncology Group (CCG 9931). Int J Radiat Oncol Biol Phys; 2009 Jul 15;74(4):1006-11
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  • [Title] A phase II study of preradiotherapy chemotherapy followed by hyperfractionated radiotherapy for newly diagnosed high-risk medulloblastoma/primitive neuroectodermal tumor: a report from the Children's Oncology Group (CCG 9931).
  • PURPOSE: To verify feasibility and monitor progression-free survival and overall survival in children with high-risk medulloblastoma and noncerebellar primitive neuroectodermal tumors (PNETs) treated in a Phase II study with preradiotherapy chemotherapy (CHT) followed by high-dose, hyperfractionated craniospinal radiotherapy (CSRT).
  • METHODS AND MATERIALS: Eligibility criteria included age >3 years at diagnosis, medulloblastoma with either high M stage and/or >1.5 cm(2) postoperative residual disease, and all patients with noncerebellar PNET.
  • Treatment was initiated with five alternating monthly cycles of CHT (A [cisplatin, cyclophosphamide, etoposide, and vincristine], B [carboplatin and etoposide], A, B, and A) followed by hyperfractionated CSRT (40 Gy) with a boost to the primary tumor (72 Gy) given in twice-daily 1-Gy fractions.
  • No significant differences were detected in subset analysis related to response to CHT, site of primary tumor, postoperative residual disease, or M stage.

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  • (PMID = 19356859.001).
  • [ISSN] 1879-355X
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA003888-44; United States / NCI NIH HHS / CA / U10 CA003888; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / U10 CA003888-44
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; BG3F62OND5 / Carboplatin; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ NIHMS128135; NLM/ PMC2739055
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65. Daniel RA, Rozanska AL, Mulligan EA, Drew Y, Thomas HD, Castelbuono DJ, Hostomsky Z, Plummer ER, Tweddle DA, Boddy AV, Clifford SC, Curtin NJ: Central nervous system penetration and enhancement of temozolomide activity in childhood medulloblastoma models by poly(ADP-ribose) polymerase inhibitor AG-014699. Br J Cancer; 2010 Nov 9;103(10):1588-96
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  • [Title] Central nervous system penetration and enhancement of temozolomide activity in childhood medulloblastoma models by poly(ADP-ribose) polymerase inhibitor AG-014699.
  • BACKGROUND: Temozolomide shows activity against medulloblastoma, the most common malignant paediatric brain tumour.
  • Poly(ADP-ribose) polymerase (PARP) inhibitors enhance temozolomide activity in extracranial adult and paediatric human malignancies.
  • METHODS: We assessed the effect of AG-014699, a clinically active PARP inhibitor, on temozolomide-induced growth inhibition in human medulloblastoma models.
  • RESULTS: Sensitivity to temozolomide in vitro was consistent with methylguanine methyltransferase (MGMT) and DNA mismatch repair (MMR) status; MGMT(+) MMR(+) D384Med cells (temozolomide GI(50)=220 μM), representative of most primary medulloblastomas, were sensitised fourfold by AG-014699; MGMT⁻ MMR(+) D425Med cells were hypersensitive (GI(50)=9 μM) and not sensitised by AG-014699, whereas MGMT(+) MMR⁻ temozolomide-resistant D283Med cells (GI₅₀=807 μM) were sensitised 20-fold.
  • AG-014699 was not toxic, accumulated and reduced PARP activity ≥75% in xenograft and brain tissues.
  • CONCLUSION: We show for the first time central nervous system penetration and inhibition of brain PARP activity by AG-014699.

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  • (PMID = 20978505.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / / C8464/A5414; United Kingdom / Department of Health / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Indoles; 0 / Poly(ADP-ribose) Polymerase Inhibitors; 7GR28W0FJI / Dacarbazine; 8237F3U7EH / rucaparib; 85622-93-1 / temozolomide; EC 2.4.2.30 / PARP1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Other-IDs] NLM/ PMC2990587
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66. Weller M: [Chemotherapy for brain tumors in adult patients]. Nervenarzt; 2008 Feb;79(2):231-41
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  • [Title] [Chemotherapy for brain tumors in adult patients].
  • Chemotherapy has become a third major treatment option for patients with brain tumors, in addition to surgery and radiotherapy.
  • Outside such clinical trials chemotherapy is used in addition to radiotherapy, e.g., in anaplastic astrocytoma, medulloblastoma or germ cell tumors, or as an alternative to radiotherapy, e.g., in anaplastic oligodendroglial tumors or low-grade gliomas.
  • Primary cerebral lymphomas are probably the only brain tumors which can be cured by chemotherapy alone and only by chemotherapy.
  • The chemotherapy of brain metastases follows the recommendations for the respective primary tumors.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Glioma / drug therapy. Lymphoma / drug therapy
  • [MeSH-minor] Adult. Chemotherapy, Adjuvant. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. Combined Modality Therapy. DNA Methylation. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Dacarbazine / adverse effects. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Genetic Markers / genetics. Humans. Prognosis. Promoter Regions, Genetic / genetics. Topotecan / adverse effects. Topotecan / therapeutic use. Tumor Suppressor Proteins / genetics

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  • (PMID = 18253773.001).
  • [ISSN] 0028-2804
  • [Journal-full-title] Der Nervenarzt
  • [ISO-abbreviation] Nervenarzt
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Genetic Markers; 0 / Tumor Suppressor Proteins; 7GR28W0FJI / Dacarbazine; 7M7YKX2N15 / Topotecan; 85622-93-1 / temozolomide; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
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67. Goldhoff P, Warrington NM, Limbrick DD Jr, Hope A, Woerner BM, Jackson E, Perry A, Piwnica-Worms D, Rubin JB: Targeted inhibition of cyclic AMP phosphodiesterase-4 promotes brain tumor regression. Clin Cancer Res; 2008 Dec 1;14(23):7717-25
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  • [Title] Targeted inhibition of cyclic AMP phosphodiesterase-4 promotes brain tumor regression.
  • PURPOSE: As favorable outcomes from malignant brain tumors remain limited by poor survival and treatment-related toxicity, novel approaches to cure are essential.
  • Here, we investigate the role of PDE4 in brain tumors and examine the utility of PDE4 as a therapeutic target.
  • EXPERIMENTAL DESIGN: Immunohistochemistry was used to evaluate the expression pattern of a subfamily of PDE4, PDE4A, in multiple brain tumor types.
  • To evaluate the effect of PDE4A on growth, a brain-specific isoform, PDE4A1 was overexpressed in xenografts of Daoy medulloblastoma and U87 glioblastoma cells.
  • RESULTS: We found that PDE4A is expressed in medulloblastoma, glioblastoma, oligodendroglioma, ependymoma, and meningioma.
  • Moreover, when PDE4A1 was overexpressed in Daoy medulloblastoma and U87 glioblastoma cells, in vivo doubling times were significantly shorter for PDE4A1-overexpressing xenografts compared with controls.
  • Bioluminescence imaging indicated that whereas temozolomide and radiation therapy arrested intracranial tumor growth, the addition of Rolipram to this regimen resulted in tumor regression.
  • CONCLUSIONS: This study shows that PDE4 is widely expressed in brain tumors and promotes their growth and that inhibition with Rolipram overcomes tumor resistance and mediates tumor regression.

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  • (PMID = 19047098.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA094056; United States / NINDS NIH HHS / NS / P30 NS057105; United States / NCI NIH HHS / CA / P30 CA91842; United States / NCI NIH HHS / CA / P30 CA091842; United States / NCI NIH HHS / CA / R21 CA108677; United States / NCI NIH HHS / CA / P50 CA94056; United States / NCI NIH HHS / CA / P50 CA094056-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Phosphodiesterase Inhibitors; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 3.1.4.17 / Cyclic Nucleotide Phosphodiesterases, Type 4; K676NL63N7 / Rolipram
  • [Other-IDs] NLM/ NIHMS82831; NLM/ PMC2615415
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68. Ellert-Miklaszewska A, Grajkowska W, Gabrusiewicz K, Kaminska B, Konarska L: Distinctive pattern of cannabinoid receptor type II (CB2) expression in adult and pediatric brain tumors. Brain Res; 2007 Mar 16;1137(1):161-9
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  • [Title] Distinctive pattern of cannabinoid receptor type II (CB2) expression in adult and pediatric brain tumors.
  • The efficacy of cannabinoids against high-grade glioma in animal models, mediated by two specific receptors, CB1 and CB2, raised promises for targeted treatment of the most frequent and malignant primary brain tumors.
  • Unlike the abundantly expressed CB1, the CB2 receptor shows a restricted distribution in normal brain.
  • Although brain tumors constitute the second most common malignancy in children and the prevalence of histological types of brain tumors vary significantly between the adult and pediatric populations, cannabinoid receptor expression in pediatric tumors remains unknown.
  • In the present study, we compared the expression of the CB2 receptor in paraffin-embedded sections from primary brain tumors of adult and pediatric patients.
  • Most glioblastomas expressed very high levels of CB2 receptors and the expression correlated with tumor grade.
  • In contrast, all examined cases of embryonal tumors (medulloblastoma and S-PNET), the most frequently diagnosed malignant brain tumors in childhood, showed no or trace CB2 immunoreactivity.
  • Our results suggest that the CB2 receptor expression depends primarily on the histopathological origin of the brain tumor cells and differentiation state, reflecting the tumor grade.
  • [MeSH-major] Brain Neoplasms / metabolism. Gene Expression Regulation, Neoplastic / physiology. Receptor, Cannabinoid, CB2 / metabolism
  • [MeSH-minor] Adolescent. Adult. Age Factors. Astrocytoma / metabolism. Child. Glioblastoma / metabolism. Histocompatibility Antigens / metabolism. Humans. Immunohistochemistry. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 17239827.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Histocompatibility Antigens; 0 / Receptor, Cannabinoid, CB2
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69. Chargari C, Feuvret L, Levy A, Lamproglou I, Assouline A, Hemery C, Ghorbal L, Lopez S, Tep B, G GB, Lang P, Laigle-Donadey F, Cornu P, Mazeron JJ, Simon JM: Reappraisal of clinical outcome in adult medulloblastomas with emphasis on patterns of relapse. Br J Neurosurg; 2010 Aug;24(4):460-7
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  • [Title] Reappraisal of clinical outcome in adult medulloblastomas with emphasis on patterns of relapse.
  • BACKGROUND: Clinical outcome and prognostic factors were assessed in adult medulloblastoma patients, with emphasis on patterns of relapse.
  • PATIENTS AND METHODS: Records of 36 consecutive adult patients with medulloblastoma were reviewed.
  • [MeSH-major] Cerebellar Neoplasms / pathology. Medulloblastoma / pathology. Neoplasm Recurrence, Local / pathology
  • [MeSH-minor] Adolescent. Adult. Chemotherapy, Adjuvant / methods. Disease-Free Survival. Female. Humans. Magnetic Resonance Angiography. Male. Middle Aged. Outcome Assessment (Health Care). Prognosis. Radiotherapy, Adjuvant / methods. Young Adult

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  • (PMID = 20726753.001).
  • [ISSN] 1360-046X
  • [Journal-full-title] British journal of neurosurgery
  • [ISO-abbreviation] Br J Neurosurg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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70. Kieran MW, Walker D, Frappaz D, Prados M: Brain tumors: from childhood through adolescence into adulthood. J Clin Oncol; 2010 Nov 10;28(32):4783-9
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  • [Title] Brain tumors: from childhood through adolescence into adulthood.
  • Clinical care is currently divided into adult or pediatric care; adolescent patients require specific expertise that most clinical practices do not have.
  • When illness coincides with the adolescent transition, the health system is severely challenged.
  • Health systems historically have varied widely in the age they choose for allocating an individual to the adult model of health care.
  • Tumors of the CNS complicate the difficult adjustments required in adolescents and young adults by virtue of their morbidity, complex treatment, and prognosis.
  • Some brain tumors are unique to children, some occur predominantly in adults, and others peak in adolescence.
  • Delays in the diagnosis of brain tumors can occur at any age but are particularly common in adolescence because of difficulties of accessing health systems, the difficulties of discriminating pathologic from typical adolescent behavioral characteristics, and changing endocrine function.
  • This article will discuss the changing brain tumor profile of children, adolescents, and adults, with a focus on our limited understanding of the adolescent/young adult transition period.
  • [MeSH-major] Brain Neoplasms / diagnosis
  • [MeSH-minor] Adolescent. Adolescent Medicine. Adult. Brain / growth & development. Child. Continuity of Patient Care. Glioma / diagnosis. Glioma / therapy. Humans. Medulloblastoma / diagnosis. Medulloblastoma / therapy. Neoplasms, Germ Cell and Embryonal / diagnosis. Neoplasms, Germ Cell and Embryonal / therapy

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  • (PMID = 20458039.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
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71. Takei H, Bhattacharjee MB, Rivera A, Dancer Y, Powell SZ: New immunohistochemical markers in the evaluation of central nervous system tumors: a review of 7 selected adult and pediatric brain tumors. Arch Pathol Lab Med; 2007 Feb;131(2):234-41
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  • [Title] New immunohistochemical markers in the evaluation of central nervous system tumors: a review of 7 selected adult and pediatric brain tumors.
  • CONTEXT: Immunohistochemistry (IHC) has become an important tool in the diagnosis of brain tumors.
  • We discuss (1) placental alkaline phosphatase, c-Kit, and OCT4 for germinoma, (2) alpha-inhibin and D2-40 for capillary hemangioblastoma, (3) phosphohistone-H3 (PHH3), MIB-1/Ki-67, and claudin-1 for meningioma, (4) PHH3, MIB-1/Ki-67, and p53 for astrocytoma, (5) synaptophysin, microtubule-associated protein 2, neurofilament protein, and neuronal nuclei for medulloblastoma, (6) INI1 for atypical teratoid/rhabdoid tumor, and (7) epithelial membrane antigen for ependymoma.
  • All the markers presented here are used mainly for supporting or confirming the diagnosis, with the exception of the proliferation markers (MIB-1/Ki-67 and PHH3), which are primarily used to support grading and are reportedly associated with prognosis in certain categories of brain tumors.
  • In addition, IHC is also of great help in predicting the prognosis for certain brain tumors.
  • [MeSH-major] Biomarkers, Tumor / analysis. Central Nervous System Neoplasms / diagnosis. Central Nervous System Neoplasms / metabolism. Immunohistochemistry
  • [MeSH-minor] Adult. Antibodies. Astrocytoma / diagnosis. Astrocytoma / metabolism. Child. Diagnosis, Differential. Ependymoma / diagnosis. Ependymoma / metabolism. Germinoma / diagnosis. Germinoma / metabolism. Hemangioblastoma / diagnosis. Hemangioblastoma / metabolism. Humans. Medulloblastoma / diagnosis. Medulloblastoma / metabolism. Meningioma / diagnosis. Meningioma / metabolism. Rhabdoid Tumor / diagnosis. Rhabdoid Tumor / metabolism

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  • (PMID = 17284108.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Biomarkers, Tumor
  • [Number-of-references] 96
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72. Privitera G, Acquaviva G, Ettorre GC, Spatola C: Antiangiogenic therapy in the treatment of recurrent medulloblastoma in the adult: case report and review of the literature. J Oncol; 2009;2009:247873

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  • [Title] Antiangiogenic therapy in the treatment of recurrent medulloblastoma in the adult: case report and review of the literature.
  • Medulloblastoma is a rare tumor in central nervous system, with an even rarer occurrence in adulthood.
  • We report the case of a 51-year-old man with recurrent medulloblastoma.
  • The aim of this report is to show that recurrent medulloblastoma in adults can be approached with a multimodality treatment and that antiangiogenic therapy should have a role in the management of this disease.

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  • (PMID = 20111585.001).
  • [ISSN] 1687-8469
  • [Journal-full-title] Journal of oncology
  • [ISO-abbreviation] J Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2804042
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73. Korshunov A, Remke M, Werft W, Benner A, Ryzhova M, Witt H, Sturm D, Wittmann A, Schöttler A, Felsberg J, Reifenberger G, Rutkowski S, Scheurlen W, Kulozik AE, von Deimling A, Lichter P, Pfister SM: Adult and pediatric medulloblastomas are genetically distinct and require different algorithms for molecular risk stratification. J Clin Oncol; 2010 Jun 20;28(18):3054-60
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  • [Title] Adult and pediatric medulloblastomas are genetically distinct and require different algorithms for molecular risk stratification.
  • PURPOSE: Medulloblastoma (MB) is the most common malignant brain tumor in children, whereas it rarely presents in adults.
  • We aimed to identify genetic aberrations in 146 adult MBs to evaluate age-dependent differences in tumor biology and adapt age-specific risk stratification models.
  • METHODS: As a screening set, we studied a cohort of 34 adult MBs by using array-based comparative genomic hybridization comparing molecular results with clinical data.
  • DNA copy number aberrations identified as possible prognostic markers were validated in an independent cohort of 112 adult patients with MB by fluorescent in situ hybridization analysis.
  • RESULTS: CDK6 amplification, 10q loss, and 17q gain are the most powerful prognostic markers in adult MB.
  • Whereas MYC/MYCN oncogene amplifications had a high prognostic value in pediatric MB, these aberrations were rarely observed in adult tumors.
  • Surprisingly, adult MBs with 6q deletion and nuclear beta-catenin activation did not share the excellent prognosis with their pediatric counterparts.
  • CONCLUSION: Adult MB is distinct from pediatric MB in terms of genomic aberrations and their impact on clinical outcomes.
  • Therefore, adult MBs require age-specific risk stratification models.
  • We propose a molecular staging system involving three distinct risk groups based on DNA copy number status of 10q and 17q.
  • [MeSH-major] Cerebellar Neoplasms / genetics. Chromosome Aberrations. Medulloblastoma / genetics. Nuclear Proteins / genetics. Oncogene Proteins / genetics. Proto-Oncogene Proteins c-myc / genetics
  • [MeSH-minor] Adolescent. Adult. Algorithms. Biomarkers, Tumor / genetics. Carcinoma, Large Cell / classification. Carcinoma, Large Cell / genetics. Carcinoma, Large Cell / metabolism. Child. Child, Preschool. Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 17 / genetics. Chromosomes, Human, Pair 6 / genetics. Comparative Genomic Hybridization. Female. Humans. Immunoenzyme Techniques. In Situ Hybridization, Fluorescence. Infant. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Prognosis. Risk Assessment. Tissue Array Analysis. Young Adult. beta Catenin / genetics

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  • (PMID = 20479417.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MYC protein, human; 0 / MYCN protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins; 0 / Proto-Oncogene Proteins c-myc; 0 / beta Catenin
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74. Lai R: Survival of patients with adult medulloblastoma: a population-based study. Cancer; 2008 Apr 1;112(7):1568-74
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  • [Title] Survival of patients with adult medulloblastoma: a population-based study.
  • BACKGROUND: Adult medulloblastoma accounts for less than 1% of adult intracranial tumors.
  • RESULTS: Four hundred fifty-four patients with adult medulloblastoma were diagnosed from 1973-2004 in the 17 regions covered by SEER.
  • [MeSH-major] Cerebellar Neoplasms / mortality. Medulloblastoma / mortality
  • [MeSH-minor] Adult. Cohort Studies. Female. Follow-Up Studies. Humans. Male. Prognosis. Registries. SEER Program. Survival Rate

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  • (PMID = 18278809.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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75. Lasky JL 3rd, Choe M, Nakano I: Cancer stem cells in pediatric brain tumors. Curr Stem Cell Res Ther; 2009 Dec;4(4):298-305
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  • [Title] Cancer stem cells in pediatric brain tumors.
  • Central nervous system (CNS) tumors remain the leading cause of death among pediatric neoplasms.
  • Although standard therapies cure many pediatric CNS tumors, the long-term cognitive and physical consequences of these therapies are devastating.
  • Although recent studies have focused on molecular mechanisms that underlie the initiation and progression of adult glioblastoma multiforme (GBM), these tumors differ phenotypically and at a molecular level from pediatric brain tumors.
  • Recent investigations have identified a stem cell population, termed "brain tumor stem cells" (BTSC) within the heterogeneous cell populations that comprise malignant brain tumors which may be partly responsible for the resistance to current therapies.
  • These have been identified in several pediatric tumors including medulloblastoma, ependymomas, and malignant gliomas.
  • By exploiting molecular differences present within these heterogeneous populations of brain tumor cells, we may be able to achieve specific eradication of BTSC and long-lasting remissions, while causing less toxicity to normal tissues.
  • In this review, we describe the issues surrounding the identification and characterization of BTSC, the molecular biology of BTSC for different pediatric brain tumors, and suggest future avenues for the development of treatments for this devastating disease.
  • [MeSH-major] Brain Neoplasms / pathology. Ependymoma / pathology. Medulloblastoma / pathology. Neoplastic Stem Cells / pathology. Optic Nerve Glioma / pathology
  • [MeSH-minor] Adult Stem Cells / pathology. Biomarkers / metabolism. Cell Differentiation. Chemotherapy, Adjuvant. Child. Humans. Surgical Procedures, Operative


76. Kao CL, Chiou SH, Ho DM, Chen YJ, Liu RS, Lo CW, Tsai FT, Lin CH, Ku HH, Yu SM, Wong TT: Elevation of plasma and cerebrospinal fluid osteopontin levels in patients with atypical teratoid/rhabdoid tumor. Am J Clin Pathol; 2005 Feb;123(2):297-304
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  • [Title] Elevation of plasma and cerebrospinal fluid osteopontin levels in patients with atypical teratoid/rhabdoid tumor.
  • Osteopontin, a cancer metastasis-associated gene, is specifically up-regulated in central nervous system (CNS) atypical teratoid/rhabdoid tumor (AT/RT), but its biological behavior in the progression of CNS AT/RT has never been studied.
  • We obtained plasma, cerebrospinal fluid (CSF), and brain tissue specimens from lobectomy or hemispherectomy samples from 39 patients (medulloblastoma, 16; AT/RT, 8; epilepsy, 6; hydrocephalus, 9).
  • By enzyme-linked immunosorbent assay, the median osteopontin levels in plasma and CSF in AT/RT (852.0 and 1,175.0 ng/mL, respectively) were significantly higher than in medulloblastoma (492.5 and 524.5 ng/mL, respectively) and hydrocephalus and epilepsy (208.0 and 168.0 ng/mL, respectively) (P < .05).
  • The results of real-time reverse transcriptase-polymerase chain reaction and immunohistochemical analysis demonstrated that osteopontin expression in AT/RT (n = 5) was significantly higher than in medulloblastoma (n = 8) samples.
  • The differences in osteopontin expression in plasma, CSF, and tumor samples in AT/RT and medulloblastoma correlated with survival differences.
  • [MeSH-major] Brain Neoplasms / metabolism. Rhabdoid Tumor / metabolism. Sialoglycoproteins. Teratoma / metabolism
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Enzyme-Linked Immunosorbent Assay. Humans. Infant. Infant, Newborn. Medulloblastoma / metabolism. Medulloblastoma / mortality. Medulloblastoma / pathology. Neoplasm Recurrence, Local. Osteopontin. Survival Rate

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  • (PMID = 15842057.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / SPP1 protein, human; 0 / Sialoglycoproteins; 106441-73-0 / Osteopontin
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77. Hänninen MM, Haapasalo J, Haapasalo H, Fleming RE, Britton RS, Bacon BR, Parkkila S: Expression of iron-related genes in human brain and brain tumors. BMC Neurosci; 2009;10:36
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  • [Title] Expression of iron-related genes in human brain and brain tumors.
  • BACKGROUND: Defective iron homeostasis may be involved in the development of some diseases within the central nervous system.
  • Although the expression of genes involved in normal iron balance has been intensively studied in other tissues, little is known about their expression in the brain.
  • We investigated the mRNA levels of hepcidin (HAMP), HFE, neogenin (NEO1), transferrin receptor 1 (TFRC), transferrin receptor 2 (TFR2), and hemojuvelin (HFE2) in normal human brain, brain tumors, and astrocytoma cell lines.
  • The specimens included 5 normal brain tissue samples, 4 meningiomas, one medulloblastoma, 3 oligodendrocytic gliomas, 2 oligoastrocytic gliomas, 8 astrocytic gliomas, and 3 astrocytoma cell lines.
  • In most tumor types, the pattern of gene expression was diverse.
  • Notable findings include high expression of transferrin receptor 1 in the hippocampus and medulla oblongata compared to other brain regions, low expression of HFE in normal brain with elevated HFE expression in meningiomas, and absence of hepcidin mRNA in astrocytoma cell lines despite expression in normal brain and tumor specimens.
  • CONCLUSION: These results indicate that several iron-related genes are expressed in normal brain, and that their expression may be dysregulated in brain tumors.
  • [MeSH-major] Brain / metabolism. Brain Neoplasms / metabolism. Gene Expression Regulation, Neoplastic / physiology. Histocompatibility Antigens Class I / metabolism. Membrane Proteins / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD / genetics. Antigens, CD / metabolism. Antimicrobial Cationic Peptides / genetics. Antimicrobial Cationic Peptides / metabolism. Astrocytoma / genetics. Astrocytoma / metabolism. Cell Line, Tumor. Female. GPI-Linked Proteins. Hepcidins. Humans. Male. Meningioma / genetics. Meningioma / metabolism. Middle Aged. Oligodendroglioma / genetics. Oligodendroglioma / metabolism. RNA, Messenger / analysis. Receptors, Transferrin / genetics. Receptors, Transferrin / metabolism. Statistics, Nonparametric. Young Adult

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  • (PMID = 19386095.001).
  • [ISSN] 1471-2202
  • [Journal-full-title] BMC neuroscience
  • [ISO-abbreviation] BMC Neurosci
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antimicrobial Cationic Peptides; 0 / CD71 antigen; 0 / GPI-Linked Proteins; 0 / HAMP protein, human; 0 / HFE protein, human; 0 / HFE2 protein, human; 0 / Hepcidins; 0 / Histocompatibility Antigens Class I; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / Receptors, Transferrin; 0 / TFR2 protein, human; 0 / neogenin
  • [Other-IDs] NLM/ PMC2679039
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78. Merchant TE, Pollack IF, Loeffler JS: Brain tumors across the age spectrum: biology, therapy, and late effects. Semin Radiat Oncol; 2010 Jan;20(1):58-66
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  • [Title] Brain tumors across the age spectrum: biology, therapy, and late effects.
  • The clinical difference between brain tumors in adults and children is striking.
  • Compared with adults, pediatric tumor types (mostly glial and neuronal) are more sensitive to adjuvant irradiation and chemotherapy.
  • In this review of glioma, ependymoma, and medulloblastoma, we highlight the differences between adults and children, including the higher incidence of spinal cord ependymoma and supratentorial high-grade glioma in the adult and a higher incidence of medulloblastoma in the child.
  • In some settings, the radiation oncologist should suggest further surgery or additional adjuvant therapy in an effort to optimize local tumor control.
  • An effort is underway to better characterize adult and pediatric brain tumors biologically with an emphasis on improving our understanding of tumor genesis, malignant transformation, and some of the similarities and differences between tumor types and their response to conventional therapy.
  • [MeSH-major] Brain Neoplasms / epidemiology. Brain Neoplasms / therapy. Glioma / epidemiology. Glioma / therapy. Radiotherapy / adverse effects
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Child. Child, Preschool. Combined Modality Therapy / methods. Disease Progression. Ependymoma / epidemiology. Ependymoma / therapy. Humans. Incidence. Infant. Infant, Newborn. Medulloblastoma / epidemiology. Medulloblastoma / therapy. Radiation Injuries. Young Adult

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  • (PMID = 19959032.001).
  • [ISSN] 1532-9461
  • [Journal-full-title] Seminars in radiation oncology
  • [ISO-abbreviation] Semin Radiat Oncol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 40
  • [Other-IDs] NLM/ NIHMS425593; NLM/ PMC3529408
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79. Karkouri M, Zafad S, Khattab M, Benjaafar N, El Kacemi H, Sefiani S, Kettani F, Dey S, Soliman AS: Epidemiologic profile of pediatric brain tumors in Morocco. Childs Nerv Syst; 2010 Aug;26(8):1021-7
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  • [Title] Epidemiologic profile of pediatric brain tumors in Morocco.
  • INTRODUCTION: Brain tumors are the most common solid tumors diagnosed among children below 15 years worldwide.
  • However, little is known about the profile of pediatric brain tumors in Africa.
  • The purpose of this study was to further elaborate the epidemiological profile of pediatric brain tumors in Africa, specifically Morocco.
  • METHODS: A retrospective review was conducted of all patients with primary brain tumors in the age group 0-19 years, from 2003 to 2007, from multiple centers in two cities of Rabat and Casablanca, Morocco.
  • Descriptive epidemiologic profiles were created for the patients by age, sex, and histological subtypes of brain tumors.
  • RESULTS: Overall medulloblastoma was the most common brain tumor (34.5%), followed by pilocytic astrocytoma (17.3%) and diffuse astrocytoma grade 2 (12.5%).
  • Brain tumors occurred most commonly in 5-9-year age group followed by 10-14-year age group with the former being more common among males and the latter being more common among females.
  • We also found medulloblastoma to be the most common brain tumor in the 0-14-year-olds.
  • CONCLUSIONS: In this rare study focused on pediatric brain tumors in Morocco, most of the findings were consistent with past studies from other parts of the world.
  • However, we found medulloblastoma to be the most common pediatric brain tumor followed by astrocytoma.
  • [MeSH-major] Brain Neoplasms / epidemiology. Brain Neoplasms / pathology
  • [MeSH-minor] Adolescent. Age Distribution. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Male. Morocco / epidemiology. Retrospective Studies. Young Adult

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  • (PMID = 20179946.001).
  • [ISSN] 1433-0350
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R25 CA112383; United States / NCI NIH HHS / CA / R25 CA112383
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Germany
  • [Other-IDs] NLM/ NIHMS649757; NLM/ PMC4276037
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80. Nakano I, Masterman-Smith M, Saigusa K, Paucar AA, Horvath S, Shoemaker L, Watanabe M, Negro A, Bajpai R, Howes A, Lelievre V, Waschek JA, Lazareff JA, Freije WA, Liau LM, Gilbertson RJ, Cloughesy TF, Geschwind DH, Nelson SF, Mischel PS, Terskikh AV, Kornblum HI: Maternal embryonic leucine zipper kinase is a key regulator of the proliferation of malignant brain tumors, including brain tumor stem cells. J Neurosci Res; 2008 Jan;86(1):48-60
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  • [Title] Maternal embryonic leucine zipper kinase is a key regulator of the proliferation of malignant brain tumors, including brain tumor stem cells.
  • Emerging evidence suggests that neural stem cells and brain tumors regulate their proliferation via similar pathways.
  • Here we describe how MELK expression is correlated with pathologic grade of brain tumors, and its expression levels are significantly correlated with shorter survival, particularly in younger glioblastoma patients.
  • In primary cultures from human glioblastoma and medulloblastoma, MELK knockdown by siRNA results in inhibition of the proliferation and survival of these tumors.
  • These results demonstrate a critical role for MELK in the proliferation of brain tumors, including their stem cells, and suggest that MELK may be a compelling molecular target for treatment of high-grade brain tumors.
  • [MeSH-major] Brain Neoplasms / pathology. Cell Proliferation. Glioblastoma / pathology. Neoplastic Stem Cells / physiology. Protein-Serine-Threonine Kinases / physiology
  • [MeSH-minor] Adult. Aged. Animals. Cells, Cultured. Female. Flow Cytometry / methods. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. Mass Spectrometry / methods. Mice. Mice, Knockout. Middle Aged. Pituitary Adenylate Cyclase-Activating Polypeptide / deficiency. RNA, Small Interfering / pharmacology. Receptors, Cell Surface / deficiency. Transfection / methods

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  • (PMID = 17722061.001).
  • [ISSN] 0360-4012
  • [Journal-full-title] Journal of neuroscience research
  • [ISO-abbreviation] J. Neurosci. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA108633; United States / NCI NIH HHS / CA / CA110384; United States / NCI NIH HHS / CA / CA88173; United States / NICHD NIH HHS / HD / HD34475; United States / NINDS NIH HHS / NS / NS050151; United States / NINDS NIH HHS / NS / NS43147
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adcyap1 protein, mouse; 0 / Pituitary Adenylate Cyclase-Activating Polypeptide; 0 / RNA, Small Interfering; 0 / Receptors, Cell Surface; 0 / patched receptors; EC 2.7.1.- / MELK protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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81. Bowers DC, Adhikari S, El-Khashab YM, Gargan L, Oeffinger KC: Survey of long-term follow-up programs in the United States for survivors of childhood brain tumors. Pediatr Blood Cancer; 2009 Dec 15;53(7):1295-301
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  • [Title] Survey of long-term follow-up programs in the United States for survivors of childhood brain tumors.
  • INTRODUCTION: Despite recognition that childhood brain tumor survivors often suffer multiple late effects following therapy, little is known regarding the long-term follow-up (LTFU) programs for these patients.
  • Institutions were asked about the size of their brain tumor program, activities of the LTFU programs and perceived barriers to follow-up.
  • Institutions with a neuro-oncology LTFU clinic were more likely to use neuro-psychological testing following radiation therapy (P = 0.001), have longer duration of continued surveillance imaging (P = 0.02), use growth hormone replacement for medulloblastoma survivors (P < 0.001) and continue the use of growth hormone into adulthood (P = 0.05) than those with a general pediatric oncology program.
  • Perceived barriers to care of brain tumor survivors included limited access and lack of insurance (32.1%), lack of funding or dedicated time for providers (22.9%), patients' uncertainty about need to follow-up (20.6%), and patients' desire to not be followed in a pediatric cancer program (12.2%).
  • CONCLUSIONS: Considerable variation exists across institutions in the United States in the delivery of follow-up care for survivors of childhood brain tumors.
  • We encourage additional investigation to better define and implement optimal follow-up care for childhood brain tumor survivors.
  • [MeSH-major] Aftercare / organization & administration. Ambulatory Care / organization & administration. Brain Neoplasms. Oncology Service, Hospital / organization & administration. Outpatient Clinics, Hospital / organization & administration. Survivors
  • [MeSH-minor] Adult. Brain Diseases / etiology. Child. Chronic Disease. Cranial Irradiation / adverse effects. Data Collection. Dwarfism, Pituitary / etiology. Dwarfism, Pituitary / prevention & control. Female. Follow-Up Studies. Human Growth Hormone / administration & dosage. Human Growth Hormone / therapeutic use. Humans. Insurance Benefits. Male. Medulloblastoma / complications. Neuropsychological Tests. Patient Participation. Radiation Injuries / drug therapy. Radiation Injuries / etiology. Societies, Medical. United States / epidemiology

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  • (PMID = 19688835.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone
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82. Sciubba DM, Gallia GL, Recinos P, Garonzik IM, Clatterbuck RE: Intracranial aneurysm following radiation therapy during childhood for a brain tumor. Case report and review of the literature. J Neurosurg; 2006 Aug;105(2 Suppl):134-9
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  • [Title] Intracranial aneurysm following radiation therapy during childhood for a brain tumor. Case report and review of the literature.
  • In this report the authors describe a 24-year-old man in whom a distal middle cerebral artery aneurysm developed 15 years after radiotherapy, which was given as adjuvant treatment following resection of a medulloblastoma.
  • [MeSH-major] Cerebellar Neoplasms / radiotherapy. Intracranial Aneurysm / etiology. Medulloblastoma / radiotherapy. Radiotherapy / adverse effects
  • [MeSH-minor] Adult. Cerebral Angiography. Humans. Magnetic Resonance Imaging. Male. Middle Cerebral Artery / pathology. Middle Cerebral Artery / surgery

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  • (PMID = 16922075.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 29
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83. Spreafico F, Gandola L, Marchianò A, Simonetti F, Poggi G, Adduci A, Clerici CA, Luksch R, Biassoni V, Meazza C, Catania S, Terenziani M, Musumeci R, Fossati-Bellani F, Massimino M: Brain magnetic resonance imaging after high-dose chemotherapy and radiotherapy for childhood brain tumors. Int J Radiat Oncol Biol Phys; 2008 Mar 15;70(4):1011-9
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  • [Title] Brain magnetic resonance imaging after high-dose chemotherapy and radiotherapy for childhood brain tumors.
  • PURPOSE: Brain necrosis or other subacute iatrogenic reactions has been recognized as a potential complication of radiotherapy (RT), although the possible synergistic effects of high-dose chemotherapy and RT might have been underestimated.
  • METHODS AND MATERIALS: We reviewed the clinical and radiologic data of 49 consecutive children with malignant brain tumors treated with high-dose thiotepa and autologous hematopoietic stem cell rescue, preceded or followed by RT.
  • RESULTS: Of the 49 children, 18 (6 of 25 with high-grade gliomas and 12 of 24 with primitive neuroectodermal tumors) had abnormal brain MRI findings occurring a median of 8 months (range, 2-39 months) after RT and beginning to regress a median of 13 months (range, 2-26 months) after onset.
  • Such findings pose a major diagnostic challenge in terms of their differential diagnosis vis-à-vis recurrent tumor.
  • [MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Brain. Brain Neoplasms. Glioma. Neuroectodermal Tumors, Primitive. Thiotepa / adverse effects
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Cognition / drug effects. Cognition / radiation effects. Combined Modality Therapy / adverse effects. Combined Modality Therapy / methods. Disease-Free Survival. Female. Humans. Infant. Intelligence / drug effects. Intelligence / radiation effects. Magnetic Resonance Imaging. Male. Medulloblastoma / drug therapy. Medulloblastoma / radiotherapy

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  • (PMID = 17904307.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 905Z5W3GKH / Thiotepa
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84. Lindsey JC, Lusher ME, Strathdee G, Brown R, Gilbertson RJ, Bailey S, Ellison DW, Clifford SC: Epigenetic inactivation of MCJ (DNAJD1) in malignant paediatric brain tumours. Int J Cancer; 2006 Jan 15;118(2):346-52
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  • [Title] Epigenetic inactivation of MCJ (DNAJD1) in malignant paediatric brain tumours.
  • We examined the status of MCJ in intracranial primitive neuroectodermal tumours [PNETs, comprising cerebellar PNETs (medulloblastomas) and supratentorial PNETs (stPNETs)] and ependymomas, together representing the most common malignant brain tumours of childhood.
  • Evidence of MCJ hypermethylation was found in all 3 tumour types [medulloblastomas, 3/9 (33%) cell lines, 2/28 (7%) primary tumours; stPNETs, 2/2 (100%) cell lines, 3/10 (30%) primary tumours; and ependymomas, 2/20 (10%) primary tumours] but not in nonneoplastic brain tissues (n = 11), indicating that MCJ methylation is a tumour-specific event.
  • Extensive methylation patterns were associated with the methylation-dependent transcriptional silencing of MCJ in medulloblastoma and stPNET cell lines.
  • These data indicate that epigenetic inactivation of MCJ may play a role in the development of a range of paediatric brain tumour types, and its role in disease pathogenesis and chemotherapeutic resistance should now be investigated further.
  • [MeSH-major] Brain Neoplasms / genetics. Ependymoma / genetics. Epigenesis, Genetic. HSP40 Heat-Shock Proteins / biosynthesis. Membrane Proteins / biosynthesis. Neuroectodermal Tumors, Primitive / genetics
  • [MeSH-minor] Adolescent. Adult. Biomarkers, Tumor. Child. Child, Preschool. DNA Methylation. Female. Gene Expression Profiling. Gene Silencing. Humans. Male. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16049974.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNAJC1 protein, human; 0 / HSP40 Heat-Shock Proteins; 0 / Membrane Proteins
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85. Pang JC, Chang Q, Chung YF, Teo JG, Poon WS, Zhou LF, Kong X, Ng HK: Epigenetic inactivation of DLC-1 in supratentorial primitive neuroectodermal tumor. Hum Pathol; 2005 Jan;36(1):36-43
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  • [Title] Epigenetic inactivation of DLC-1 in supratentorial primitive neuroectodermal tumor.
  • Supratentorial primitive neuroectodermal tumors (SPNETs) and medulloblastomas (MBs) are histologically similar intracranial tumors found in different anatomic locations of the brain.
  • The aim of this study was to evaluate whether DLC-1, a newly identified tumor-suppressor gene on chromosome 8p22, is involved in the tumorigenesis of MBs and the histologically similar SPNETs.
  • Bisulfite sequencing further verified a densely methylated pattern of 35 CpG sites studied in M1 that were not found in normal brain, indicating that inactivation of DLC-1 by hypermethylation is involved in SPNET.
  • [MeSH-major] Epigenesis, Genetic. Gene Silencing. Neuroectodermal Tumors, Primitive / genetics. Supratentorial Neoplasms / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Adolescent. Adult. Base Sequence. Cell Line, Tumor. Cerebellar Neoplasms / genetics. Child. Child, Preschool. Chromosomes, Human, Pair 8 / genetics. CpG Islands. DNA Methylation. Female. GTPase-Activating Proteins. Gene Expression Regulation, Neoplastic. Humans. Infant. Lasers. Loss of Heterozygosity. Male. Medulloblastoma / genetics. Microdissection. Molecular Sequence Data. Promoter Regions, Genetic. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15712180.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DLC1 protein, human; 0 / GTPase-Activating Proteins; 0 / Tumor Suppressor Proteins
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86. Malakootian M, Mowla SJ, Saberi H, Asadi MH, Atlasi Y, Shafaroudi AM: Differential expression of nucleostemin, a stem cell marker, and its variants in different types of brain tumors. Mol Carcinog; 2010 Sep;49(9):818-25
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  • [Title] Differential expression of nucleostemin, a stem cell marker, and its variants in different types of brain tumors.
  • In the present study, we have examined the expression of NS and its spliced variants in various brain tumors.
  • Total RNA was extracted from 59 brain tumor samples, and the expression of different NS spliced variants was measured by semi-quantitative RT-PCR.
  • The subcellular distribution of NS protein in brain tumors was further examined by immunohistochemistry.
  • Furthermore, to decipher the potential involvement of NS in brain tumorogenesis, its expression was knocked-down by means of RNA interference (RNAi) in two malignant glioma (U-87MG and A172), one astrocytoma (1321N1) and one medulloblastoma (DAOY) cell lines.
  • Our data revealed that NS and its variants are widely expressed in different types of brain tumors.
  • Among the NS spliced variants, variant "1" and variant "3" were detected in the majority of tumor samples, whereas variant "2" was only detectable in few samples.
  • As expected, a nucleolar/nucleoplasmic localization of NS protein was observed in the examined tumor samples.
  • All in all, our data suggest a potential role for NS in tumorogenesis of brain cancers.
  • [MeSH-major] Astrocytoma / metabolism. Brain Neoplasms / genetics. Brain Neoplasms / metabolism. Glioma / metabolism
  • [MeSH-minor] Adult. Brain / metabolism. Cell Cycle / genetics. Cell Line. Cell Proliferation. Female. Humans. Immunohistochemistry. Male. Medulloblastoma / genetics. Medulloblastoma / metabolism. Medulloblastoma / pathology. Middle Aged. Proteins / genetics. Proteins / metabolism. RNA Interference. RNA Splicing. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Stem Cells / metabolism. Stem Cells / pathology

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  • [Copyright] 2010 Wiley-Liss, Inc.
  • (PMID = 20572164.001).
  • [ISSN] 1098-2744
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proteins; 0 / RNA, Small Interfering
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87. Pogoda JM, Preston-Martin S, Howe G, Lubin F, Mueller BA, Holly EA, Filippini G, Peris-Bonet R, McCredie MR, Cordier S, Choi W: An international case-control study of maternal diet during pregnancy and childhood brain tumor risk: a histology-specific analysis by food group. Ann Epidemiol; 2009 Mar;19(3):148-60
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  • [Title] An international case-control study of maternal diet during pregnancy and childhood brain tumor risk: a histology-specific analysis by food group.
  • PURPOSE: Maternal dietary data from an international collaborative case-control study on childhood brain tumors were used to evaluate associations between histology-specific risk and consumption of specific food groups during pregnancy.
  • Other histology-specific associations were decreased risk of anaplastic astrocytomas from cruciferous vegetables (OR, 0.4; 95% CI, 0.3-0.7 for 4th vs. 1st quartile; p trend<0.0001), decreased risk of astroglial tumors from fresh fish (OR, 0.6; 95% CI, 0.5-0.9 for 4th vs. 1st quartile; p trend=0.008), and increased risk of medulloblastoma from oil products (OR, 1.5; 95% CI, 1.0-2.2 for 4th vs. 1(st) quartile; p trend=0.005).
  • CONCLUSIONS: These results suggest the need for dietary analysis not only by brain tumor histology, but also by specific foods within a broad food group.

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  • (PMID = 19216997.001).
  • [ISSN] 1873-2585
  • [Journal-full-title] Annals of epidemiology
  • [ISO-abbreviation] Ann Epidemiol
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES007048; United States / NCI NIH HHS / CA / P01 CA017054-30; United States / NCI NIH HHS / PC / N01 PC035139; United States / NCI NIH HHS / CA / CA47082; United States / NIEHS NIH HHS / ES / P30 ES007048-029003; United States / NCI NIH HHS / CA / CA47081; United States / NCI NIH HHS / CA / CA17054; United States / NCI NIH HHS / CN / N01-CN-05230; United States / NIEHS NIH HHS / ES / ES007048-029003; United States / NCI NIH HHS / CN / N01-CN-25403; United States / NCI NIH HHS / CA / P01 CA017054; United States / NCI NIH HHS / CA / N01 CN025403; United States / NCI NIH HHS / CN / N01 CN005230; United States / NIEHS NIH HHS / ES / 5P30 ES07048
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nitroso Compounds
  • [Other-IDs] NLM/ NIHMS98974; NLM/ PMC2832584
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88. Rollison DE, Utaipat U, Ryschkewitsch C, Hou J, Goldthwaite P, Daniel R, Helzlsouer KJ, Burger PC, Shah KV, Major EO: Investigation of human brain tumors for the presence of polyomavirus genome sequences by two independent laboratories. Int J Cancer; 2005 Feb 20;113(5):769-74
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  • [Title] Investigation of human brain tumors for the presence of polyomavirus genome sequences by two independent laboratories.
  • JC virus (JCV), BK virus (BKV) and simian virus 40 (SV40) may be associated with human brain tumors.
  • These polyomaviruses have been shown to induce brain tumors in experimentally infected animals.
  • Several studies have found polyomavirus genomic sequences in human brain tumor tissues by using polymerase chain reaction (PCR), while others have not.
  • To assess the role of polyomaviruses in human brain tumors and address inconsistencies of previous reports, we investigated the prevalence of viral sequences in a series of 225 brain tumor tissue specimens in 2 independent laboratories.
  • The JHU laboratory amplified DNA from 165/225 (73%) tumors, of which 1 tumor tested positive (for SV40).
  • Nucleotide sequences for JCV, BKV and SV40 are rarely present in a large series of adult and pediatric brain tumors.
  • [MeSH-major] Brain Neoplasms / virology. Polyomavirus Infections / virology. Tumor Virus Infections / virology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. BK Virus / genetics. BK Virus / isolation & purification. Blotting, Southern. Child. Child, Preschool. DNA, Neoplasm / genetics. Female. Genome, Viral. Glioma / diagnosis. Glioma / genetics. Glioma / virology. Humans. Infant. JC Virus / genetics. JC Virus / isolation & purification. Male. Medulloblastoma / diagnosis. Medulloblastoma / genetics. Medulloblastoma / virology. Meningioma / diagnosis. Meningioma / genetics. Meningioma / virology. Middle Aged. Polymerase Chain Reaction. RNA, Messenger / genetics. RNA, Viral / genetics. Reverse Transcriptase Polymerase Chain Reaction. Simian virus 40 / genetics. Simian virus 40 / isolation & purification

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  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15499616.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / RNA, Messenger; 0 / RNA, Viral
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89. Wang Z, Fan QH, Yu MN, Zhang WM: [Clinicopathologic and immunohistochemical study of atypical teratoid/rhabdoid tumor of central nervous system]. Zhonghua Bing Li Xue Za Zhi; 2006 Aug;35(8):458-61
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  • [Title] [Clinicopathologic and immunohistochemical study of atypical teratoid/rhabdoid tumor of central nervous system].
  • OBJECTIVE: To study the clinicopathologic features and differential diagnosis of atypical teratoid/rhabdoid tumor (AT/RT) occurring in the central nervous system.
  • The tumor cells were positive for vimentin, CD99, epithelial membrane antigen, cytokeratin, glial fibrillary acidic protein, S-100 protein, neurofilament, desmin and smooth muscle actin.
  • CONCLUSIONS: AT/RT is a highly malignant tumor occurring in the central nervous system.
  • It manifests mainly in children and occasionally in adults.
  • The tumor is characterized by a heterogeneous histologic and immunohistochemical phenotype.
  • It needs to be distinguished from a number of central nervous system tumors, including medulloblastoma, primitive neuroectodermal tumor, germ cell neoplasm and rhabdoid meningioma.
  • [MeSH-major] Brain Neoplasms / pathology. Rhabdoid Tumor / pathology. Teratoma / pathology
  • [MeSH-minor] Actins / analysis. Adult. Antigens, CD / analysis. Cell Adhesion Molecules / analysis. Child, Preschool. Desmin / analysis. Glial Fibrillary Acidic Protein / analysis. Humans. Immunohistochemistry. Keratins / analysis. Male. Mucin-1 / analysis. Muscle, Smooth / chemistry. Neurofilament Proteins / analysis. S100 Proteins / analysis. Vimentin / analysis

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  • (PMID = 17069697.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Actins; 0 / Antigens, CD; 0 / CD99 protein, human; 0 / Cell Adhesion Molecules; 0 / Desmin; 0 / Glial Fibrillary Acidic Protein; 0 / Mucin-1; 0 / Neurofilament Proteins; 0 / S100 Proteins; 0 / Vimentin; 68238-35-7 / Keratins
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90. Panosyan EH, Laks DR, Masterman-Smith M, Mottahedeh J, Yong WH, Cloughesy TF, Lazareff JA, Mischel PS, Moore TB, Kornblum HI: Clinical outcome in pediatric glial and embryonal brain tumors correlates with in vitro multi-passageable neurosphere formation. Pediatr Blood Cancer; 2010 Oct;55(4):644-51
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  • [Title] Clinical outcome in pediatric glial and embryonal brain tumors correlates with in vitro multi-passageable neurosphere formation.
  • BACKGROUND: Cultured brain tumors can form neurospheres harboring tumorigenic cells with self renewal and differentiation capacities.
  • Renewable neurosphere formation has clinical predictive value in adult malignant gliomas, yet its prognostic role for pediatric brain tumors is unknown.
  • Overall survival (OS) was significantly worse for neurosphere-forming patients with embryonal tumors, as a group and amongst the subgroup with medulloblastoma, but not in the glial group.
  • CONCLUSIONS: Neurosphere formation is more predictive of pediatric brain tumor progression than semi-quantitative Ki67 staining.
  • Pediatric brain tumor derived neurospheres may provide a predictive model for preclinical explorations.

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  • [Copyright] Copyright 2010 Wiley-Liss, Inc.
  • [Cites] J Clin Oncol. 2003 Dec 15;21(24):4572-8 [14673044.001]
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  • (PMID = 20589659.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS052563; United States / NCI NIH HHS / CA / T32 CA009056; United States / NCI NIH HHS / CA / U54 CA119347; United States / NINDS NIH HHS / NS / R01NS052563
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS572199; NLM/ PMC4017922
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91. Kremer P, Fardanesh M, Ding R, Pritsch M, Zoubaa S, Frei E: Intraoperative fluorescence staining of malignant brain tumors using 5-aminofluorescein-labeled albumin. Neurosurgery; 2009 Mar;64(3 Suppl):ons53-60; discussion ons60-1
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  • [Title] Intraoperative fluorescence staining of malignant brain tumors using 5-aminofluorescein-labeled albumin.
  • OBJECTIVE: The newly developed conjugate 5-aminofluorescein (AFL)-human serum albumin (HSA) was investigated in a clinical trial for fluorescence-guided surgery of malignant brain tumors to assess its efficacy and tolerability.
  • The extent of tumor resection was verified by early postoperative magnetic resonance imaging.
  • RESULTS: Fluorescence staining of tumor tissue was bright in 11 patients (84%), resulting in complete resection of fluorescent tumor tissue in 9 patients (69%).
  • In 2 patients, residual fluorescent tumor tissue was also confirmed by magnetic resonance imaging.
  • Neither bleaching nor penetration of AFL-HSA into the surrounding brain edema or into necrotic tissue was seen.
  • The agreement between fluorescence and histopathology in tumor samples and samples of the tumor border was 83.3%.
  • CONCLUSION: Tumor fluorescence using AFL-HSA made fluorescence-guided brain tumor resection possible, demonstrating that albumin is a suitable carrier system for selective targeting of aminofluorescein into malignant gliomas.
  • [MeSH-major] Brain Neoplasms / pathology. Fluoresceins. Glioma / pathology. Serum Albumin
  • [MeSH-minor] Adult. Aged. Cell Proliferation. Female. Glioblastoma / pathology. Glioblastoma / surgery. Humans. Logistic Models. Magnetic Resonance Imaging. Male. Medulloblastoma / pathology. Medulloblastoma / surgery. Microscopy, Fluorescence. Middle Aged. Oligodendroglioma / pathology. Oligodendroglioma / surgery. Paraffin Embedding. Tissue Fixation

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  • (PMID = 19240573.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fluoresceins; 0 / Serum Albumin; 3326-34-9 / 5-aminofluorescein
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92. Zhou Y, Liu F, Xu Q, Wang X: Analysis of the expression profile of Dickkopf-1 gene in human glioma and the association with tumor malignancy. J Exp Clin Cancer Res; 2010;29:138
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  • [Title] Analysis of the expression profile of Dickkopf-1 gene in human glioma and the association with tumor malignancy.
  • BACKGROUND: Gliomas represent the most common primary malignant brain tumors, yet little is known about the molecular pathogenesis of these tumors.
  • The aim of this study was to examine the expression profile of DKK-1 gene in human glioma and its association with tumor malignancy.
  • METHODS: We determined the expression levels of DKK-1 transcript and protein in 12 glioblastoma cell lines, medulloblastoma cells, low-grade glioma cells, and human astrocyte cells by semiquantitative RT-PCR and ELISA.
  • A total of 47 tumor biopsy specimens and 11 normal brain tissue samples from patients with cerebral trauma internal decompression were embedded in paraffin blocks and used for immunostaining.
  • Twenty-six primary tumors and 7 corresponding brain samples were stored in liquid nitrogen and used for RT-PCR.
  • RESULTS: DKK-1 could only be detected in 12 human glioblastoma cell lines, not in a panel of other tumor and normal cell lines.
  • Kendall's tau-c association analysis also revealed the increased DKK-1 protein expression in tumor tissues of higher pathologic classification.
  • The levels of cerebral fluid DKK-1 protein were significantly higher in glioma patients than in healthy donors or in neuronal benign tumor patients, suggesting that the DKK-1 molecule in cerebral fluids can be applicable to detect the presence of glioma and be developed as a novel prognostic treatment.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain Neoplasms / genetics. Gene Expression Profiling. Glioma / genetics. Intercellular Signaling Peptides and Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Enzyme-Linked Immunosorbent Assay. Female. Gene Expression. Humans. Immunohistochemistry. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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  • (PMID = 21029453.001).
  • [ISSN] 1756-9966
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DKK1 protein, human; 0 / Intercellular Signaling Peptides and Proteins
  • [Other-IDs] NLM/ PMC2990739
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93. Barnholtz-Sloan JS, Severson RK, Stanton B, Hamre M, Sloan AE: Pediatric brain tumors in non-Hispanics, Hispanics, African Americans and Asians: differences in survival after diagnosis. Cancer Causes Control; 2005 Jun;16(5):587-92
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  • [Title] Pediatric brain tumors in non-Hispanics, Hispanics, African Americans and Asians: differences in survival after diagnosis.
  • BACKGROUND: Racial differences in survival for children with brain tumors have not been well studied, particularly in Hispanics and Asians.
  • The objective of this study was to assess racial differences in survival of children with brain tumors, focusing on Hispanics, African Americans and Asians compared to Non-Hispanics.
  • METHODS: Subjects identified through the SEER Program were 2799 children, < or =19 years old at diagnosis, newly diagnosed between 1973 and 1996 with primary, malignant brain tumors.
  • Kaplan-Meier models and Cox proportional hazards models were used to assess racial differences in overall survival and in survival by histological type of tumor.
  • RESULTS: The distribution histological type of tumor varied significantly by race.
  • Overall survival was similar for Hispanics, African Americans, Asians compared to Non-Hispanics, although trends of increased risk of death for the minority groups were noted when stratifying by histological type of tumor.
  • CONCLUSIONS: Racial differences in survival could exist by histological type of tumor, but further work is necessary for a more complete understanding of these differences.
  • [MeSH-major] Brain Neoplasms / mortality. Continental Population Groups / statistics & numerical data
  • [MeSH-minor] Adolescent. Adult. Astrocytoma / ethnology. Astrocytoma / mortality. Astrocytoma / therapy. Child. Child, Preschool. Ependymoma / ethnology. Ependymoma / mortality. Ependymoma / therapy. Female. Humans. Infant. Infant, Newborn. Male. Medulloblastoma / ethnology. Medulloblastoma / mortality. Medulloblastoma / therapy. Proportional Hazards Models. SEER Program. Survival Analysis. United States / epidemiology

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  • (PMID = 15986114.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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94. Eskandary H, Sabba M, Khajehpour F, Eskandari M: Incidental findings in brain computed tomography scans of 3000 head trauma patients. Surg Neurol; 2005 Jun;63(6):550-3; discussion 553
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  • [Title] Incidental findings in brain computed tomography scans of 3000 head trauma patients.
  • We studied the frequency of incidental findings on 3000 brain CT scans of trauma patients.
  • METHODS: Three thousands standard brain CT scans of trauma patients were evaluated for some incidental findings.
  • RESULTS: In this study we found 30 incidental abnormalities that include 8 cases of tumor: 3 meningioma, 2 craniopharyngioma, 1 oligodendroglioma, 1 low-grade astrocytoma, and 1 medulloblastoma.
  • Three suspect lipomas were found in midline and near midline of the brain.
  • CONCLUSION: Cisterna magna enlargement was the most common incidental finding and brain tumor and arachnoid cyst were next in frequency.
  • [MeSH-major] Brain / radiography. Brain Diseases / radiography. Brain Neoplasms / radiography. Craniocerebral Trauma / radiography. Tomography, X-Ray Computed / statistics & numerical data
  • [MeSH-minor] Adolescent. Adult. Aged. Arachnoid Cysts / pathology. Arachnoid Cysts / radiography. Calcinosis / pathology. Calcinosis / radiography. Child. Child, Preschool. Comorbidity. Cross-Sectional Studies. Female. Humans. Hydrocephalus / pathology. Hydrocephalus / radiography. Infant. Infant, Newborn. Male. Middle Aged. Prevalence


95. Kieran MW, Packer RJ, Onar A, Blaney SM, Phillips P, Pollack IF, Geyer JR, Gururangan S, Banerjee A, Goldman S, Turner CD, Belasco JB, Broniscer A, Zhu Y, Frank E, Kirschmeier P, Statkevich P, Yver A, Boyett JM, Kun LE: Phase I and pharmacokinetic study of the oral farnesyltransferase inhibitor lonafarnib administered twice daily to pediatric patients with advanced central nervous system tumors using a modified continuous reassessment method: a Pediatric Brain Tumor Consortium Study. J Clin Oncol; 2007 Jul 20;25(21):3137-43
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  • [Title] Phase I and pharmacokinetic study of the oral farnesyltransferase inhibitor lonafarnib administered twice daily to pediatric patients with advanced central nervous system tumors using a modified continuous reassessment method: a Pediatric Brain Tumor Consortium Study.
  • PURPOSE: A dose-escalation phase I and pharmacokinetic study of the farnesyltransferase inhibitor lonafarnib (SCH66336) was conducted in children with recurrent or progressive CNS tumors.
  • RESULTS: Fifty-three children with progressive or recurrent brain tumors were enrolled, with a median age of 12.2 years (range, 3.9 to 19.5 years).
  • Both radiographic response (one anaplastic astrocytoma) and stable disease (one medulloblastoma, two high-grade and four low-grade gliomas, one ependymoma, and one sarcoma) were noted, and seven patients remained on treatment for 1 year or longer.
  • [MeSH-major] Central Nervous System Neoplasms / drug therapy. Central Nervous System Neoplasms / mortality. Enzyme Inhibitors / pharmacokinetics. Farnesyltranstransferase / antagonists & inhibitors. Neoplasm Invasiveness / pathology. Piperidines / pharmacokinetics. Pyridines / pharmacokinetics
  • [MeSH-minor] Administration, Oral. Adolescent. Adult. Child. Child, Preschool. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Infant. Infant, Newborn. Male. Maximum Tolerated Dose. Neoplasm Staging. Risk Assessment. Survival Analysis. Treatment Outcome

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  • (PMID = 17634493.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01 CA81457
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Piperidines; 0 / Pyridines; 193275-84-2 / lonafarnib; EC 2.5.1.29 / Farnesyltranstransferase
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96. Furneaux CE, Marshall ES, Yeoh K, Monteith SJ, Mews PJ, Sansur CA, Oskouian RJ, Sharples KJ, Baguley BC: Cell cycle times of short-term cultures of brain cancers as predictors of survival. Br J Cancer; 2008 Nov 18;99(10):1678-83
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  • [Title] Cell cycle times of short-term cultures of brain cancers as predictors of survival.
  • Brain tumour material obtained at surgery from 70 patients with glioblastoma, medulloblastoma, astrocytoma, oligodendroglioma and metastatic melanoma was cultured for 7 days on 96-well plates, coated with agarose to prevent proliferation of fibroblasts.
  • For patients with brain cancers of all types, median survival for the < or =10-day and >10-day groups were 5.1 and 12.5 months, respectively (P=0.0009).
  • Lower grade gliomas had longer median culture cycle times (16 days) than those of medulloblastomas (9.9 days), glioblastomas (9.8 days) or melanomas (6.7 days).
  • We conclude that culture cycle times determined using short-term cultures of surgical material from brain tumours correlate with patient survival.
  • [MeSH-major] Brain Neoplasms / physiopathology. Cell Cycle
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Female. Humans. Kinetics. Male. Middle Aged. Prognosis. Survival Analysis. Time Factors. Tumor Cells, Cultured

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  • (PMID = 18854836.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2584938
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97. Jacobs AH, Thomas A, Kracht LW, Li H, Dittmar C, Garlip G, Galldiks N, Klein JC, Sobesky J, Hilker R, Vollmar S, Herholz K, Wienhard K, Heiss WD: 18F-fluoro-L-thymidine and 11C-methylmethionine as markers of increased transport and proliferation in brain tumors. J Nucl Med; 2005 Dec;46(12):1948-58
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  • [Title] 18F-fluoro-L-thymidine and 11C-methylmethionine as markers of increased transport and proliferation in brain tumors.
  • Because of the high glucose metabolism in normal brain tissue 18F-FDG is not the ideal tracer for the detection of gliomas.
  • Methyl-11C-l-methionine (11C-MET) is better suited for imaging the extent of gliomas, because it is transported specifically into tumors but only insignificantly into normal brain.
  • 3'-Deoxy-3'-18F-fluorothymidine (18F-FLT) has been introduced as a proliferation marker in a variety of neoplasias and has promising potential for the detection of brain tumors, because its uptake in normal brain is low.
  • Kinetic modeling was performed on 14 patients for regional time-activity curves of 18F-FLT from tumorous and normal brain tissue.
  • Tumor volumes detected by 18F-FLT and 11C-MET were larger than tumor regions displaying gadolinium enhancement (P<0.01).
  • Some tumor regions were detected only by either 18F-FLT (7 patients) or 11C-MET (13 patients).
  • Kinetic modeling revealed that 18F-FLT uptake in tumor tissue seems to be predominantly due to elevated transport and net influx.
  • CONCLUSION: 18F-FLT is a promising tracer for the detection and characterization of primary central nervous system tumors and might help to differentiate between low- and high-grade gliomas.
  • In some tumors and tumor areas, 18F-FLT uptake is not related to 11C-MET uptake.
  • [MeSH-major] Antiviral Agents / pharmacology. Astrocytoma / radionuclide imaging. Brain Neoplasms / radionuclide imaging. Dideoxynucleosides / pharmacology. Glioma / radionuclide imaging. Medulloblastoma / radionuclide imaging. Methionine / analogs & derivatives. Radiopharmaceuticals / pharmacology
  • [MeSH-minor] Adult. Aged. Biological Transport. Cell Proliferation. False Positive Reactions. Female. Humans. Kinetics. Magnetic Resonance Imaging / methods. Male. Middle Aged. Phosphorylation. Positron-Emission Tomography. Sensitivity and Specificity. Time Factors

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  • (PMID = 16330557.001).
  • [ISSN] 0161-5505
  • [Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine
  • [ISO-abbreviation] J. Nucl. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Dideoxynucleosides; 0 / Radiopharmaceuticals; AE28F7PNPL / Methionine; BN630929UL / methionine methyl ester; PG53R0DWDQ / alovudine
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98. Perry A, Miller CR, Gujrati M, Scheithauer BW, Zambrano SC, Jost SC, Raghavan R, Qian J, Cochran EJ, Huse JT, Holland EC, Burger PC, Rosenblum MK: Malignant gliomas with primitive neuroectodermal tumor-like components: a clinicopathologic and genetic study of 53 cases. Brain Pathol; 2009 Jan;19(1):81-90
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  • [Title] Malignant gliomas with primitive neuroectodermal tumor-like components: a clinicopathologic and genetic study of 53 cases.
  • Central nervous system neoplasms with combined features of malignant glioma and primitive neuroectodermal tumor (MG-PNET) are rare, poorly characterized, and pose diagnostic as well as treatment dilemmas.
  • Anaplasia, as seen in medulloblastomas, was noted in 70%.
  • (ii) may represent a metaplastic process or expansion of a tumor stem/progenitor cell clone;.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Agents, Alkylating / therapeutic use. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Brain Neoplasms / therapy. Combined Modality Therapy. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Female. Follow-Up Studies. Genes, myc / genetics. Humans. In Situ Hybridization, Fluorescence. Medulloblastoma / genetics. Medulloblastoma / pathology. Medulloblastoma / therapy. Neoplasm Metastasis. Neoplasms, Multiple Primary / genetics. Neoplasms, Multiple Primary / pathology. Neoplasms, Multiple Primary / therapy. Prognosis. Radiotherapy / methods. Treatment Outcome. Young Adult

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  • (PMID = 18452568.001).
  • [ISSN] 1750-3639
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Proto-Oncogene Proteins; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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99. Barnes M, Eberhart CG, Collins R, Tihan T: Expression of p75NTR in fetal brain and medulloblastomas: evidence of a precursor cell marker and its persistence in neoplasia. J Neurooncol; 2009 Apr;92(2):193-201

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of p75NTR in fetal brain and medulloblastomas: evidence of a precursor cell marker and its persistence in neoplasia.
  • p75 neurotrophin receptor (p75NTR) is a member of the tumor necrosis factor superfamily, and plays a significant role in nervous system development. p75NTR has a dual (proliferative/apoptotic) role in neurogenesis and binds pro-neurotrophins with high affinity.
  • Recent work suggests p75NTR is overexpressed in the developing cerebellum and in nodular/desmoplastic medulloblastomas.
  • We analyzed p75NTR expression in various parts of the fetal and adult human central nervous system, and in 75 patients with medulloblastomas.
  • The expression of p75NTR in the fetal brain was seen solely within the external granular layer with weaker expression in the Purkinje layer, which most likely represents Purkinje cell staining.
  • The staining was present in gestational weeks 20-40, while no staining was identified elsewhere in the fetal brain or within the adult cerebellum. p75NTR positive cells were also positive with the proliferation marker ki-67, but were negative for ret, reelin, CD133, CD34, and cleaved caspase 3.
  • Nine of 75 medulloblastomas (12%) were also showed positive immunostaining for p75NTR.
  • The staining was seen in four classic, two desmoplastic, and three anaplastic medulloblastomas.
  • The persistence of p75NTR in a small group of medulloblastomas raises the possibility that in such tumors, the receptor could be a potential therapeutic target.
  • [MeSH-major] Biomarkers, Tumor / analysis. Brain / metabolism. Cerebellar Neoplasms / metabolism. Medulloblastoma / metabolism. Receptor, Nerve Growth Factor / biosynthesis

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  • (PMID = 19066726.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptor, Nerve Growth Factor
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100. Blamek S, Wydmański J, Sokół M, Matulewicz L, Boguszewicz L: Magnetic resonance spectroscopic evaluation of brain tissue metabolism after irradiation for pediatric brain tumors in long-term survivors: a report of two cases. Acta Neurochir Suppl; 2010;106:191-4
Hazardous Substances Data Bank. CHOLINE CHLORIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Magnetic resonance spectroscopic evaluation of brain tissue metabolism after irradiation for pediatric brain tumors in long-term survivors: a report of two cases.
  • OBJECTIVE: The aim of our study was to evaluate the metabolic profile of brain tissue of two long-term survivors of childhood brain tumors.
  • MATERIALS: Two males who were 25 and 33 years old at the time of examination and had been irradiated for brain tumors at the age of 17 and 13 years respectively.
  • The first subject had been operated on radically for medulloblastoma and received craniospinal axis irradiation composed of a whole brain radiotherapy with boost to the posterior fossa (total dose (TD) = 59.4 Gy in 33 fractions) and spinal canal irradiation (TD = 30 Gy in 20 fractions) according to the protocol at the time of treatment.
  • The second subject had previously received whole brain irradiation (TD = 45 Gy in 19 fractions) because of inoperable central region tumor of unknown histology.
  • The spectra were acquired both from the tumor bed area and uninvolved brain tissue in the first subject, and from uninvolved brain areas of frontal and occipital lobes in the second subject.
  • CONCLUSIONS: Metabolic parameters correlated with neuronal function (NAA/Cr) and cell membrane metabolites turnover (Cho/Cr) seem to recover to normal values in long-term survivors of brain tumors.
  • Lac/Cr and Lip/Cr proportions could be considered parameters indicating permanent radiation-induced brain damage; however, this proposal requires further investigation.
  • [MeSH-major] Brain / metabolism. Brain / radiation effects. Brain Neoplasms / pathology. Brain Neoplasms / radiotherapy. Survivors
  • [MeSH-minor] Adolescent. Adult. Aspartic Acid / analogs & derivatives. Aspartic Acid / metabolism. Choline / metabolism. Creatine / metabolism. Humans. Lactic Acid / metabolism. Magnetic Resonance Spectroscopy / methods. Male

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • Hazardous Substances Data Bank. LACTIC ACID .
  • Hazardous Substances Data Bank. (L)-ASPARTIC ACID .
  • Hazardous Substances Data Bank. CREATINE .
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  • (PMID = 19812947.001).
  • [ISSN] 0065-1419
  • [Journal-full-title] Acta neurochirurgica. Supplement
  • [ISO-abbreviation] Acta Neurochir. Suppl.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Austria
  • [Chemical-registry-number] 30KYC7MIAI / Aspartic Acid; 33X04XA5AT / Lactic Acid; 997-55-7 / N-acetylaspartate; MU72812GK0 / Creatine; N91BDP6H0X / Choline
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